On 2020-05-13 13:19:20, user T Christopher Bond wrote:
Looking for an explanation of the total numbers and the comparator group in Table 4 (ICI vs ?).
On 2020-05-13 13:19:20, user T Christopher Bond wrote:
Looking for an explanation of the total numbers and the comparator group in Table 4 (ICI vs ?).
On 2020-05-13 18:50:12, user John wrote:
Lack of Vitamin D has been implicated, paler skin produces more, and there are potential genetic factors too, watching this may help https://youtu.be/Ja-jhcXMGj0
On 2020-05-14 05:11:14, user Matthew Ward wrote:
Hi Anne, brilliant study - Well done to all the team.
Could a saliva sample prove sensitive enough for Sars-Cov-2 to be detected on a lateral flow test?
Or would the sample almost always require amplification via PCR to increase sensitivity?
Many thanks<br /> Matt
On 2020-05-14 12:31:40, user Riccardo Pecori wrote:
Very nice work. A couple of questions for the authors: <br /> 1 - in the self-collected samples (Triton experiment) what is the volume of PBS in which the swabs are rinsed? <br /> 2 - would it be possible to get the written instructions for self-sampling? It would be beneficial for the standardization of the sampling.
On 2020-05-14 17:42:03, user MiCo BioMed wrote:
This paper makes a false claim, because the authors didn't follow MiCo Biomed's PCR test instruction.. The authors used an RNA extraction kit manufactured by Invitrogen, which is incompatible with MiCo BioMed's PCR kit. MiCo BioMed's PCR kit instruction clearly tells users to use only MiCo Biomed's RNA extraction kit.
On 2020-05-15 16:11:42, user David Simons wrote:
Please in future versions of this article consider reporting a descriptive analysis by your outcomes of interest. Saying current smokers had a 5 times greater risk of ITU admission or 10 times greater risk of death is not helpful when you are not reporting the absolute numbers.
On 2020-05-15 16:48:46, user Will Wiegman wrote:
A combo of severe Thiocyanate and Iodine Deficiencies shuts down the pitting function of the spleen making it impossible for the body to eliminate the viruses trapped inside of mature red blood cells with no nucleus for the virus to use to replicate.
https://www.ncbi.nlm.nih.go...
https://pubmed.ncbi.nlm.nih...
Paragraph 4:<br /> https://pubmed.ncbi.nlm.nih...
On 2020-05-15 22:28:30, user Sally Elghamrawy wrote:
Any one need the dataset ,,,just send to me.
On 2020-05-18 02:17:06, user welko welko wrote:
There were 33 positive IgG among 1,000 serum samples 33 per 1000<br /> so...<br /> 330 per 10,000<br /> 3300 per 100,000<br /> 4950 per 150,000<br /> From your data I calculated; its 3.3% not 33%:Give Kobe a break
On 2020-05-19 16:06:56, user Jared Roach wrote:
The main point of this article is really good. The more variance there is in the infectiousness of individuals, the greater the probability of complete elimination. Indeed, if there is zero variance, then elimination will never occur. This assumes a fairly simple model (e.g., SIS compartmental model). The article would benefit from a few references to classical epidemiological models that the assumptions are based on. The point about animal reservoirs in the last paragraph should be more strongly emphasized. We know this virus originally came from bats, and we know that dogs and felines can be infected. So it seems very likely that there will be animal reservoirs. This point should be emphasized, with references.
On 2020-05-19 20:06:13, user Achint Chaudhary wrote:
I have gone through this and similar articles recently published.I found some issues on which I am bit skeptical about approach followed by the authors:
Data Augmentation (using SMOTE) is done before splitting the data into Train-Test sets, which will leak information from train set to test set.
Data balance is achieved on Test set also, I agree that class balanced data set will led to a better classifier, but reporting metric values on a test set with different class ratio from real world testing is an issue to be raised
XGBoost is shown to be the best known algorithm in this article, but XGBoost algorithm is already known to handle class imbalance, so why do we need SMOTE at first place. Would not it be right if experiments without data augmentation would be also shown
On 2020-05-20 06:25:22, user Bob wrote:
How do the authors reconcile a lower bound of 0.02 IFR with the fact that 0.026% of Americans have already died from SARS-CoV-2? Kind of difficult to have an IFR lower than that.
On 2020-05-23 11:05:15, user John Jacobson wrote:
It would be great to see more of a discussion on how many of the recorded deaths from COVID-19 are directly attributable to Sars-CoV-2. Is the current ~96K US deaths the true death toll of direct deaths from Covid-19 or does this number include significant number of deaths from other causes, but list Covid-19 in death certificate (e.g. a patient with renal failure or end-stage liver cancer or head trauma picks up nosocomial infection and is recorded as part of covid burden)? This would surely reduce IFR estimates if accurately known. Is testing for Covid-19 more widespread than for routine influenza A or B infections? Seems likely in the current climate in the midst of a pandemic, which might be another caveat when comparing. Important to factor in both of these points to get a greater appreciation and context of the current pandemic?
On 2020-05-20 06:50:14, user Chris Valle-Riestra wrote:
Thank you, I can see that this is a very important finding for understanding the development of the epidemic in any nation, region, or city. That heterogeneity in susceptibility would have this effect can be understood intuitively, as soon as one really starts to think about it. Determining an average R nought for an entire nation, and making projections based on that alone, plainly doesn't tell the whole story.
A simple thought experiment will demonstrate this. If an entire population is split into two sub-populations of equal size, and the individuals in one of the sub-populations all have low susceptibility, effective R just for that sub-population can be well below 1.0, in spite of a generally high virulence of the virus. Very few in this sub-population will ever become infected. The other half of the full population will be highly susceptible, and a substantial majority of that sub-population would be expected to become infected over time. Adding it all up, something well under 50% of the total population will ultimately become infected, and herd immunity will have been achieved.
Recent small serological studies around the U.S. have typically indicated a middle-of-the-road level of infection, ranging between perhaps 6 and 30 percent from place to place, many weeks into the epidemic. This has struck me as perplexing. Based on the usual naive model of the development of an epidemic, one would have thought it likely to find either (1) a very low level of infection, such as under 5 percent, implying great success in suppression efforts, or (2) infection levels moving steadily past 50 percent, implying a high R nought that suppression efforts were inadequate to suppress. Basically, either suppression would work or it wouldn't. It would be surprising to find that that the virus had enough power to infect a major fraction of the population, carrying a big head of steam going forward, and yet be able to be halted that late in the game.
Your finding points to a likely explanation for this phenomenon. It suggests to me a likelihood that the epidemic in the U.S. has been working its way through the most susceptible sub-populations, not successfully checked, but that it has made little progress in infecting less susceptible sub-populations.
I think it should be recognized that to the degree that an individual's susceptibility is based on his social conditions, that may change over time. An individual living far out in the country may have little connectivity, and therefore little susceptibility. If he moves into the heart of a city, that may change. This implies that herd immunity is likely to "erode" over time. COVID-19 is likely to remain endemic and to continue to cause a low level of disease, serious and otherwise, for a long time to come.
Be that as it may, there's a strong likelihood that public health officials and political leaders have been seriously misinterpreting the progress of epidemic. This has major implications for public policy choices. Further research is urgently needed, and decision makers need to develop a more nuanced understanding. They are currently making weighty decisions based upon a probably badly flawed model.
On 2020-05-21 01:11:37, user Brian Richard Allen wrote:
Be interesting to see how New Zealand:- whose authoritarian government has effectively prevented its subjects from acquiring herd immunity;- will fare when its borders are opened and tourists -- and the virus -- flow in.
On 2020-05-21 01:21:24, user Morat Gurgeh wrote:
This whole affair has been entirely unedifying. I do not know the truth of the allegations published in Buzzfeed, but then neither does anyone else commenting here, on Twitter and elsewhere. There are a lot of people, including senior academics, who should be ashamed of their behaviour.
Turning to the central controversy, it is entirely possible and indeed likely for different populations to have different IFRs. The fact that the IFR in NYC appears to be significantly higher than reported here does not “debunk” this work and indeed is not even inconsistent with these results.
NYC was hit early by the virus, when protocols for managing infected patients were still developing and mistakes were made. In addition, those most susceptible to COVID-19 (e.g. the old) were much less likely to be voluntarily shielding. Catastrophic errors have been made in many countries in care homes. So the likelihood of those over 80 being infected was likely much higher than in this study. Given the incredibly steep fatality gradient with age, this alone could explain the IFR differences.
I think the main take home message of this paper is this: the lives of healthy, working age people should return largely to normal while those groups identified at elevated risk should continue to shield. Amongst the young, we should treat infection by SARS-CoV-2 as more akin to measles than Ebola.
We need most of the healthy, young population to develop what immunity they can to this virus so that we can properly protect those most susceptible.
On 2020-07-21 21:41:59, user Alfred_Packer wrote:
This research was done very early, and has the imperfections inherent in such an early effort- but they appear to have been pretty close to the actual IFR. At the time it was seen as impossibly low and a dozen researchers beat this study up. So how did such a flawed study get the right answer, basically?
On 2020-04-24 07:31:44, user Dennis Menace wrote:
The children they tested were brought in by their parents. These are also not independent, is this a problem ?
On 2020-05-21 20:00:27, user Babak Javid wrote:
Please note that the Supplementary File refers to the earlier version of this manuscript and is no longer current. Unfortunately, it cannot be removed for clarity!
On 2020-05-22 23:43:28, user Malcolm Semple wrote:
Features of 20 133 UK patients in hospital with covid-19 using the ISARIC WHO Clinical Characterisation Protocol: prospective observational cohort study<br /> BMJ 2020; 369 doi: https://doi.org/10.1136/bmj... (Published 22 May 2020)<br /> Cite this as: BMJ 2020;369:m1985
On 2020-05-23 09:25:08, user Francesca Simonato wrote:
What hydrogen peroxide concentration was used?
On 2020-05-24 09:26:14, user Count Iblis wrote:
The natural vitamin D levels are way higher than the average levels found in populations living in the civilized world. Biologically normal vitamin D levels are between 120 nmol/l and 250 nmol/l. Levels below 100 nmol/l are from a natural biological point of view extremely low, but such levels are the norm in the civilized World, even in the tropics as people there too spend most of the day indoors.
Studies like this that look into the correlation between vitamin D levels naturally found in society and harmful effects of COVID-19 effect are interesting, but they cannot detect all of the effects of the severe vitamin D deprivation of the western population. It's similar to a study into the effects of exercise on heart disease if you're studying a population of couch potatoes. You may detect a difference between those couch potatoes that don't sit all day long on the couch and those that hardly get up at all during the day. But the large effects on heart health that kick in when you run for more than half an hour a day, cannot be extracted from such a study.
On 2020-05-25 11:34:54, user Rogelio Macías-Ordóñez wrote:
Even after countless revisions prior tu submission to medRxiv we found a minor mistake in the sentence (lines 375-378):
"A group of five countries (Brazil Fig 4, México, India, Peru and Russia) with IFR values below 1% and an already high death toll (above 1,000) may experience a high number of casualties if, as our estimates suggest, they experience 68-82% more deaths in the next 23 days."
It should say "...64-82% more deaths in the next 23 days." since 64% is the lowest value (for Brazil) among those countries in Table 1.
On 2020-07-17 13:12:12, user Liam Golding wrote:
What is the detection limit of this assay? I assume it's >log0.
On 2020-07-18 00:57:36, user Kamran Kadkhoda wrote:
Despite other reports such high seroprevalence in healthcare setting highly suggests false positivity. Ideally all positives should have been confirmed by neuralization assay. Since most were mild/moderate/asymptomatic and they admit 50% were confirmed this is an attestation to high false positivity of their screen test. I refer them to the large Wuhan study with 2% sero-prevalence as they confirmed all cases with neuralization. Most positives found here are probably from common CoVs...for the record specificity of 100% is a mathematical impossibility.
On 2020-07-18 08:58:40, user disqus_LHZMcrKY6P wrote:
LAMP has great potential as a screening tool, the limit of detection (100,000 c/ml ?) is at least 10 times less than most commercial and LDT assay based on traditional RT PCR methods. I note the authors suggest "If such a test were to be used for community screening outside of CLIA-certified diagnostic labs, effective interventions could be taken immediately while awaiting confirmatory tests at partner CLIA labs" When used in this way it Is a very good screening tool. It would be important in times of global supply issues and economical impact of testing versus impact to balance implications of duplication of swab collection.<br /> Those using and commissioning tests must be aware of the limitations of all assays and use them appropriately. It is very attractive to use tests that are high throughput and low cost. This assay would be well suited during peaks of pandemics where negative results are followed up by CLIA testing.
On 2020-07-18 09:38:23, user disqus_LHZMcrKY6P wrote:
Thank you for this informative paper, the statistical probabilities of result significance in the event of a negative result are very important in terms of the application of the test. Is there possibility to follow-up negative lamp results in both asymptomatic contacts and symptomatic cases with laboratory based assays RT-pcr assays (with LOD< 1000 cp/ml) and repeat LAMP assay at say 4-7 days later to evidence the statistical probabilities with true outcome? Do the authors recommend that LAMP assay result is routinely followed up with a more sensitive test for negative results?<br /> I cannot see units for analytical sensitivity is this copies/ml, per reaction or per swab? This is important for selecting a confirmatory test that has a more sensitive limit of detection and for comparing results across assay and finally for understanding the % of samples that would not be detected if this was performed as a single test based on current knowledge of viral loads in samples.<br /> The natural history of covid19 disease makes the means that interpretation of significance of low viral loads is reliant on a number of factors specific to the individual, while it is true that a low viral load is less likely to be infective, we cannot be sure at which stage of infectious course the individual is at and therefore low viral loads cannot be ruled as insignificant in terms of infectious potential nor clinical outcome.
On 2020-07-18 11:59:14, user Kevin wrote:
This paper appears to be a good quantitative assessment of the relative risk between full flights and flights with empty middle seats (~44% reduction with empty middle seats).
I believe the author’s attempt to quantify the overall probability of contracting COVID while flying to be highly flawed.
First, the Lancet study states its mask values are from (at worst) 12-ply cotton masks, and this paper assumes 100% mask compliance. Twitter is full of photos of non-compliant airline passengers, and with no federal regulations defining and requiring mask compliance, the author’s assumption skews the assessment.
Second, the author states he makes no attempt to account for duration of exposure. I assume the author believes this is acceptable, since as stated in the paper “the air in the aircraft cabin is constantly refreshed, so the cabin does not constitute a closed indoor space.” Unfortunately, FAA Regulation 25.831 (a) specifies a minimum fresh air volume requirement, but allows that to be mixed with filtered recirculated air. So while better than a room with no fresh air being circulated, it is not the same as standing in an open field. Again, not taking exposure time into account likely skews the outcome to make air travel appear safer than it is.
Third, and this may be the most important, the author does nothing to account for arguably the highest risk activities while aboard an aircraft: boarding and de-planing. As soon as the seatbelt light goes off, passengers jump out of their seats and crowd the aisle, huffing and puffing as they pull their suitcases out of the overhead bin, all while pressed up against fellow travelers. Boarding is a similar mess, but can at least be controlled through passenger metering at the gate and entry door. If the paper doesn’t consider the highest risk activities associated with flying, it can’t attempt to assign an overall probability to air travel.
In summary, this is not a comprehensive analysis of the probability of contracting COVID while flying, and the overall probabilities should not be presented and discussed since the underlying assumptions are both incomplete and likely flawed. This paper does appear to do good work comparing the transmission probability due to passenger proximity (QL), and should concentrate the findings in that area.
On 2020-07-19 10:16:32, user Shahar Seifer wrote:
The density of virions in aerosols may be different than the density in saliva. The argument on probability of transmission is based on the assumption that the two values are the same, which is doubtful.
On 2020-07-19 10:54:36, user C Ilie wrote:
The best way to test a theoretical model is to run an experiment. But, what if the experiment already took place? Princess Diamond Cruise analysis found the infection rate was below 20%. <br /> https://www.linkedin.com/pu...
On 2020-07-23 10:39:18, user Jeff Morris wrote:
I would love for these “dark matter” arguments to be true. I understand the mathematics, but is there any direct evidence that significant proportions of the population have immunity from exposure to previous coronaviruses or is it just hopeful speculation? Our antibody studies at Penn suggest our patient population has coronavirus antibody prevalence of about 1% — it is not even clear if these IgG titers indicate immunity — but even if they did the 1% would be negligible and big enough to produce this proposed “dark matter” effect.
On 2020-07-19 14:36:08, user Ulrich Müller-Sedgwick wrote:
Great to see this paper published with interesting results. I was the lead clinician for the CPFT Adult ADHD Clinic until March 2017 (when I moved to London). How should we screen for hoarding symptoms? Is there a screening version of longer questionnaires or 1-2 questions that we can ask in our clinical interview, especially in patients with procrastination as a main symptom?
On 2020-07-20 05:20:08, user Curbina wrote:
I have wondered if China published total mortality data that could be used as it has been done elsewhere to estimate excess mortality during the pandemic. This article is the closest to that so far.
On 2020-07-21 15:54:39, user OxImmuno Literature Initiative wrote:
On 2020-07-22 09:15:41, user Ben Berman wrote:
Is there an association with BRCA1/2 germline status? About 17% of TCGA cases are BRCA1/2 germline carriers.
On 2020-07-22 20:52:39, user Stuart Hameroff wrote:
Congratulations. I think the ultrasound mechanism of action is on microtubules and the microtubule-organizing-center (MTOC) which get hijacked by the virus for trafficking, filopdium growth to infect other cells, and cytokine storm. Ultrasound is mechanical vibrations in megahertz. Microtubules have resonance frequencies in megahertz, and cell studies show ultrasound rearranges microtubules into optimal configurations. Let's treat the microtubules on which the virus depends, e.g. those in vagus nerve, spleen and other areas. Ultrasound is painless, safe, inexpensive and widely available.
On 2020-07-23 01:12:23, user William Croft wrote:
Many reports surfacing online of reinfections (google covid reinfection). Within weeks or months of the 1st infection, after antibodies no longer exist. This would seem to caution against antibody based approaches. Unless the goal is re-vaccination every three months(!) Admittedly profitable for manufacturers. ;-)
On 2020-06-23 23:51:31, user Steve Moss wrote:
My initial concern after a very brief skim of the article, is that the raw data and statistical methods (including relevant code/parameters) aren’t available for reproducibility purposes. Could the preprint please be updated with links to these resources?
On 2020-06-24 08:42:37, user Canberk Baci wrote:
A study with a great prospect! Not only facilitates the interpretation of smears, but also provides the means of access to the opinions of specialists in this field. It would also reduce diagnostic costs.
On 2020-07-25 13:01:40, user Matthias von Davier wrote:
Something is missing here. Country level correlations can be inverse to individual level correlation (and they may be in this case). There's a long history of ecological fallacies and other types of wrong conclusions when making inferences from group level association to the individual level.
Andrew Gelman wrote https://www.amazon.com/Red-...
And the original Robinson 1950 article is here:
On 2020-07-25 15:35:31, user wbgrant wrote:
Without information on the vitamin D dose and serum 25-hydroxyvitamin D concentrations of the participants, no concluusion can be made regarding vitamin D from this study. See<br /> Grant WB. Re: Preventing a covid-19 pandemic: Can vitamin D supplementation reduce the spread of COVID-19? Try first with health care workers and first responders. BMJ. April 1, 2020 https://www.bmj.com/content...
On 2020-07-26 13:21:08, user MaverickNH wrote:
“... we have no information on whether the excess firearms acquired were those used in violence.”
With an estimated 390 million guns in civilian hands in the US, it would indeed be difficult to attribute any estimated increase in criminal use of guns to those recently purchased during the pandemic. Unless, perhaps, the motivations of the purchasers was markedly nefarious. But as these excess purchases were estimated from NICS background checks, one might infer the purchasers to be *less* likely to use guns in criminal acts. As BJS surveys of prisoners found only 1.3% obtained the guns used in their crimes by purchased from retail sources, the connection between legal excess gun purchases and criminal use of guns is very tenuous. Beyond being unable to establish a causal relationship between excess gun purchases and increased criminal use of guns, the relationship is most likely fortuitous.
On 2020-07-26 17:29:35, user Dude Dujmovic wrote:
Great, too bad samples are so small but this is worth expanding.
On 2020-07-27 06:13:06, user OxImmuno Literature Initiative wrote:
On 2020-06-26 17:52:11, user abdullah Alsultan wrote:
Thanks for the great work, few questions regarding your PK study:
1) I think in the Perinel study, they used whole blood conc not serum
2) How did you determine the blood/plasma partitioning ratio? In your study it was 1.64, prior studies was closer to ~5
3) Would be good to add to figure 1, the predicted blood conc bases on the serum conc you observed
Thanks,<br /> Abdullah Alsultan
On 2020-06-27 15:36:00, user Dr SK Gupta wrote:
Researchers have rightly pointed out that plasma works in Non intubated patients and not so in Intubated patients meaning thereby.. plasma therapy if given late in course of disease may not be effective. Intubated patients obviously meant more sick and those with advanced disease who failed to respond to nasal oxygen inhalation, High flow nasal oxygen and CPAP... <br /> (Authors may please clarify the criteria of intubation if different.)<br /> Findings are in line with the observation that once the cytokine storm has done the damage, Neutralizing antibodies in plasma may not be able to reverse it. Cytosorb or ECMO is the only modality left for such patients apart from usual care.
Good interesting finding was effectively of use of plasma with titres 1:320 while most of the studies are done with titres 1:640.<br /> Study has the limitation of using retrospective cohort as control arm. Prospective selection for inclusion in Plasma arm and retrospective selection in control arm both can increase observer bias.
Nevertheless it is important be because it may not be practically possible to take consent of sick patient to be included into placebo group depriving him of so much advertised benefits of plasma therapy.
On 2020-07-29 18:21:23, user Alen Stojanac wrote:
When I've first noticed that anomaly in charts, my first thought was on the line of some of the comments - that it had something to do with the way reports were made. But this gives far more plausible explanation. Thank you.
On 2020-07-30 06:51:21, user Marm Kilpatrick wrote:
Thank you for this important study. Could you clarify if there is a typo in both Table 1 & 2 concerning the 2nd age group? It says 25-29 in both cases, but this would mean there are no data for ages 15-24. Should the age group in both cases be 15-29?<br /> thanks,<br /> marm
On 2020-07-30 13:59:42, user Pablo Richly wrote:
Could you please provide the rational of including the Rasheed et al study in the RCT group analysis since the authors stated in their paper that "21 of the patients were randomly chosen to take CP, while other age- and sex- matched 28 patients were under the conventional therapy as control group".?
On 2020-07-30 23:33:03, user Sluggo67 wrote:
The spatial pattern of Covid 19 deaths has substantially changed since the authors last updated the manuscript. Will the manuscript be withdrawn until the statistical analysis can be updated to incorporate all of the data from this evolving global health crisis?
On 2020-06-30 12:35:03, user Dude Dujmovic wrote:
May 4 to May 12. That was sort of ages ago. OK as a snapshot I guess.
On 2020-08-01 23:31:09, user Michael Verstraeten wrote:
I would like to add 2 comments on this article.
Specific governmental instructions to family doctors on testing, providing general care and hospitalisation criteria, affect also the randomness of the used samples. Patient with general complaints, but with a suspicion of Covid - 19, were refused or postponed for other needed care so that they were excluded from testing. In this way an unknown part of the population infected with Covid - 19 was excluded from your samples.
To state that "we are still far away from natural herd immunity" and "50 - 75 % of a population would need to have protective immunity (...) in order to achieve herd immunity mitigating subsequent waves of Covid - 19", you refer to 2 publications. One from D'Arienzo a.o., and the other from Liu.Y, a.o. Neither of them discuss the phenomenon of herd immunity. Both estimated in an early stage the R0 for Covid - 19. Taking in account your remark about eventual T-cell dependent immunity and your reference to the serology in Sweden, and considering the unknowns about Covid - 19, taking also in account the natural decrease of Rt in several countries before the confinements, there is no evidence that without confinement the overall infection rates in countries would ever reach 50 - 70 %, nor that herd immunity or other forms of immunity would not limit the overall infection rate for Covid - 19 to much lower percentages comparable to the historical infection rates for Influenza pandemics.
M. Verstraeten <br /> MBA
On 2020-08-02 11:49:02, user Rosemary TATE wrote:
Excellent paper. Thank-you so much for uploading the appropriate checklist. This seems to be almost always ignored!
On 2020-08-02 15:44:56, user Paul McKeigue wrote:
This manuscript has now been accepted for publication by PLoS Medicine
On 2020-08-03 13:56:54, user Charles R. Twardy wrote:
Another preprint out today finds risk reduction above 1000m in the US. Assuming both your effects are real and causal, possibly the same mechanism?
On 2020-08-04 19:47:00, user Kamran Kadkhoda wrote:
The specificity of 85% doesn't support your conclusion...
On 2020-08-04 22:41:06, user Mark Andrew Jones wrote:
Great paper. Did you consider also looking at (or at least discussing) "harm" outcomes e.g. mental health, unemployment rates, government handouts?
On 2020-07-03 08:50:08, user Roberto Avelar wrote:
Very interesting work. Thank you for citing CellAge! Just wanted to let you know we have published our database now ( https://genomebiology.biome... )
Cheers,<br /> Roberto
On 2020-08-05 10:32:37, user Beata Fonferko-Shadrach wrote:
This is an excellent review, however, as creators of the extraction of epilepsy clinical text system (ExECT),we would like to point out that that your statement of the way ExECT annotates and extracts seizure frequency is incorrect. Your review states that “The ExECT pipeline … identified the phrase or sentence within a clinical document that contained the seizure frequency but does not return a numeric value…” In our paper we clearly say that for seizure frequency we extract “the number of seizures in a specific time period” and then we give examples of phrases e.g. “two seizures per day”, “seven seizures in a year”, or “seizure free since last seen in clinic.” (Table 1 – Details on the categories of extracted information and criteria for manual review).2 Whether stated as numbers or words, numerical values are extracted as numerals, and the time period is extracted as a time period i.e. day, week, month, year. The number of seizures extracted from the last example given is 0 with a point in time of “last clinic”. Ref (doi: 10.1136/bmjopen-2018-023232)
Beata Fonferko-Shadrach
On 2020-07-04 02:28:38, user Experimental Methods wrote:
Do you have any breathability (differential pressure) data for this combination? It is easy to get high filtration efficiency, but if the material isn't breathable enough, most air inhaled will come from the side of the mask, defeating its purpose
On 2020-08-08 20:29:03, user Yiyun Shi wrote:
will there be an issue taking the average for each individual's value when pooling across different imputation datasets in contrast to using Rubin's rule?
On 2020-07-05 14:02:12, user Nataliya Skrypnyk wrote:
It would be interesting to see the actual range of IL-13 in the both groups of patients
On 2020-07-06 16:29:22, user OxImmuno Literature Initiative wrote:
On 2020-07-07 16:30:21, user Rosemary TATE wrote:
I took a quick look at this. Looks useful, but just a couple of comments from a statistician. 1. Spearman correlation coefficients are called rho - not r (well done for using Spearman). It's the coefficient that is important so no need to report the p-value as even a small correlation will be significant whit a large number of observations. Also, you are looking at the death rates, not the numbers so need to make this clear.
On 2020-07-09 08:53:02, user Ahmed wrote:
Applying the logistic growth model to the second period (scenario) separately is unprecedented approach as modeling should include the entire data of a single outbreak. It will be useful to model (scenario 3) which includes the whole period.
On 2020-08-14 04:52:30, user Melimelo wrote:
Great paper, could you please say which hygroscopic materials you tested? (salt? rice? something else?)
On 2020-07-09 20:12:01, user scott kelley wrote:
Where is the trial with immediate treatment at time of positive test in patients over 65 without ekg abnormalities. Like all antivirals, early treatment is the key.
On 2020-08-14 22:32:38, user Andrew Foers wrote:
Really nice work, and a great resource! Looking forward to your future reports.
If I was reviewing this I'd ask for more information about the control subjects. Without details as to how the control subjects were processed, we are unable to judge if preparation differences in the control cohort contirbute to sample classification.
On 2020-07-10 21:22:21, user Dimy Fluyau wrote:
The paper presents quantitative data on the efficacy of some pharmacological classes of drugs( medications) to manage or treat benzodiazepine( BZD) withdrawal. BZD withdrawal is a life-threatening condition, and its treatment requires the immediate use of BZDs. However, beyond the use of BZD for the management of BZD withdrawal, other drugs( medications) can also manage or treat the withdrawal. Some of them present less risk of withdrawal, tolerance, or dependence. Thus, their use may be recommended.
On 2020-08-15 14:44:07, user Rakeshkumar Yadav wrote:
Which PEG was used ? PEG9000?<br /> Why the sample volume is variable and not fixed?
On 2020-07-13 09:48:00, user Rosemary TATE wrote:
Interesting, but I think the major limitation (which you do mention in the discussion) is that the "actual" number of cases is probably not that at all, due to lack of testing, or reporting. It would seem more likely that the projections for the number of cases are accurate, but the severity of symptoms is not, and so the cases are not being identified. <br /> I have never seen the following mentioned as a limitation! ".. statistical tests, p-values and confidence intervals carry their share of limitations and insufficiencies that need to be mentioned and accounted for." Could you please expand?
On 2020-07-14 04:46:01, user AJ wrote:
Interesting paper. Gives an important view of CD8 physiology following infection. As expected, but not reassuring- the CD8s are more differentiated on a background of lymphopenia. Concerning to say the least.
On 2020-07-14 12:41:27, user David Simons wrote:
There are ongoing questions about a potential protective effect of nicotine. You report tobacco use and the risk of hospitalisation which includes both current and former tobacco use. There are multiple confounders associated with these groupings (i.e. those who have increased comorbidities are more likely to be former compared to current smokers). Could you consider exploring this in further versions of your work?
On 2020-07-15 10:54:18, user quanta renormalized wrote:
I seriously wonder weather the author know the definition of power-law. Fitting any arbitrary polynomial function to a time-series data doesn't amount to a power-law.<br /> https://en.wikipedia.org/wi...
On 2020-09-07 11:05:36, user Raffaele Loffredo wrote:
Why not controlling for age distribution of cases (possibly of infected people)? In Italy and other countries the high mortality during the firs peak can be, at least partially, explained by the fact that the pandemic has been first and foremost an hospital-acquired infection. Consequently the pandemic during the firs peak has hurt the most vulnerable part of the population. This can explain the higher mortality and ICU occupacy rates during the first peak (also the harvesting effect can be at play).
On 2021-07-10 02:06:06, user Marcus wrote:
No mention of strain or variant specific data, even in limitations discussion.
On 2021-05-16 11:40:32, user ingokeck wrote:
This is a very interesting preprint, especially as they authors state the LOD which many others never give. 0.007 /ml TID50 for ORF1ab mean that you need to ingest 1ml/0.007=142 ml to have a 50% chance of infection (ignoring for one the immune protection in the mucus) at the ct vale of 33. Or, the other way round, a ct vale of 33-7 = 26 would correspond to 1ml of sample that would infect 50%. At the threshold the authors selected of ct 30, one would still need 17ml of sample to infect 50%. <br /> Also, ORF1ab is interesting because it should be much more near to the actual amount of infectious virion than for example the N-gene which gets copied many sizes of magnitude more often than the ORF1ab gene.
On 2021-05-17 21:44:07, user Red Lawhern wrote:
In your paper you write
"drug monitoring programs (PDMPs) reduce prescribing rates 8.7%, while <br /> mandatory PDMPs increase death rates from opioids 16.6%, heroin and <br /> fentanyl 19.0%, cocaine 17.3% and all drugs 10.5%"
This phrasing seems to assert demonstrated cause and effect. It is not at all clear to me that the techniques you are applying have the capability to establish that.
Likewise, there is an important question in this process that you do not address and I would hope you may be willing to attempt: recognizing that predominant modes of overdose mortality involve multiple legal and illegal opioids in the great majority of deaths, is the contribution of opioids prescribed by doctors to their patients (not diverted) statistically significant in the overall mortality rate due to all opioids, legal and illegal? Based on the relative rarity of addiction to medically managed prescription opioids, I would suggest that it is not.
Your comments are invited.
On 2021-05-18 18:17:37, user happydog wrote:
NOTE from the authors: The Brazil data used in the analysis (the data associated with the Hallal et al. (2020) serostudy; see https://doi.org/10.1016/S22... ) must be reevaluated in light of new results about the sensitivity of the Wondfo antibody tests (Silveira et al.; see: http://dx.doi.org/10.2139/s... ). We are currently working on a revised analysis with this in mind.
On 2021-05-20 03:04:05, user kdrl nakle wrote:
Your samples are way too small for sweeping conclusions you made.
On 2021-05-22 00:45:46, user Michael Plank wrote:
The model and results in this pre-print are now part of an article published in the Journal of the Royal Society of New Zealand, available open access at: https://doi.org/10.1080/030...
On 2021-05-23 07:56:10, user Sabina Pfister wrote:
Table shows significant difference in distribution of 1-2 symptoms and 3 or more symptoms between seropositive and seronegative. Yet the discussion combines the two categories into 1 or more symptoms. Looking at 3 or more symptoms separately could lead to different conclusions, with the caveat of low numbers.
On 2021-05-25 06:21:14, user japhetk wrote:
The clinical site of this trial defines case as following and positive serology alone should be counted as a case. But instead in this manuscript, positive serology is not counted as a case.
Positive serology is greater in BCG group (7/148) compared with placebo (2/153). But in the result this is apparently not counted as a case as BCG group has only 2 cases.
Primary Outcome Measures :<br /> Positive for the respiratory <br /> questionnaire consisted of questions concerning the appearance of <br /> symptoms possibly, probably and/or definitively related to COVID-19 on <br /> visit 3. [ Time Frame: Visit 3 (90 +/- 5 days) ]
This is set on visit 3 (90 ± 5 days from the date of visit 1). The two <br /> groups of vaccination are compared for the primary endpoints which is <br /> composite. Patients who meet any of the following will be considered to <br /> meet the primary endpoint:
O Positive for the respiratory questionnaire endpoint when at least one of the following <br /> combination is met either at visit 2 and/or at visit 3:
-One situation definitively related to COVID-19<br /> -All four questions of symptoms possibly related to COVID-19<br /> -At least two questions of symptoms possibly related to COVID-19 as well as need for admission at the emergency department of any hospital and/or need for intake of <br /> antibiotics<br /> -At least four questions of symptoms probably related to COVID-19 one of which is "need foradmission at the emergency department of any hospital and/or need for <br /> intake of antibiotics"
OPositive IgG or IgM antibodies against SARS-CoV-2
On 2021-05-25 14:13:52, user max wrote:
what about deep sequencing of the sperm? or snp for covid pieces?
On 2021-05-25 15:23:14, user Dinofelis wrote:
The results for Niaee are inverted between control group and ivermectin group. Control group 11 death, IVM group: 4 death. See https://www.researchsquare....
Didn't check others.
On 2021-05-27 09:29:55, user MarcWathelet wrote:
What a joke, after your "mistake" inverting the control and IVM arm of the Niaee study, the RR goes from 1.11 to 0.37 yet you dare to not change a single word in your conclusion:<br /> In comparison to SOC or placebo, IVM did not reduce all-cause mortality,<br /> length of stay or viral clearance in RCTs in COVID-19 patients with mostly mild disease.<br /> IVM did not have effect on AEs or SAEs. IVM is not a viable option to treat COVID-19<br /> patients.<br /> The new "scientists": we don't care about data contradicting our preconceived interpretation, we stick to our guns! Propaganda Abteilung!
On 2021-05-27 14:01:51, user unscientific science wrote:
Dr.Niaee posted this on the previous version of this article: Hi, I'm Dr.Niaee and I was surprised that even basic data from our RCT is completely mispresented and is WRONG. We had 60 indivisuals in control groups and 120 in intervention groups and even this simple thing is mispresrntated.
You can read all the comments to this article if you click on "View comments on earlier versions of this paper".
On 2021-05-26 09:43:39, user Laura Potts wrote:
Many thanks for this article. I appreciate this is a pre read but would be grateful for clarification as within the text it states “Age was significantly associated with Long-COVID (LC28) rising from 9.9% in 18-49 year olds to 21.9% in those aged >=70” using the data in table 1 looking at over 70s 24/96 gives 25% rather than 21.9% and the sums of the ages don’t add to the overall count for both overall and L28. It would great if these numbers could be updated.
On 2021-05-26 19:18:16, user Gudsson wrote:
This study might be crucial when explaing the susceptibility to the symptoms of Long Covid.
On 2021-05-27 06:20:33, user Mike Stevens wrote:
Well, it’s not whether there is a mandate in place, is it?<br />
It’s whether the mandate is adhered to.<br />
And when people actually comply, and wear the masks, Covid spread declines.<br />
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0249891
Funny how a disease spread primarily through droplet spread can be halted by methods that stop droplet spread, isn’t it?<br /> ...Who would have thought it?
On 2021-05-27 20:05:21, user NC91 wrote:
No one mentions the caution at the top of the article.
On 2021-05-28 12:42:16, user Barbara Elizabeth wrote:
For those who have commented here that wearing the mask (mandate or not) is what lowers numbers... another study on NIH site disagrees (and you've surely heard of this) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680614/. The conclusion states: <br /> "The existing scientific evidences challenge the safety and efficacy of wearing facemask as preventive intervention for COVID-19. The data suggest that both medical and non-medical facemasks are ineffective to block human-to-human transmission of viral and infectious disease such SARS-CoV-2 and COVID-19, supporting against the usage of facemasks. Wearing facemasks has been demonstrated to have substantial adverse physiological and psychological effects. These include hypoxia, hypercapnia, shortness of breath, increased acidity and toxicity, activation of fear and stress response, rise in stress hormones, immunosuppression, fatigue, headaches, decline in cognitive performance, predisposition for viral and infectious illnesses, chronic stress, anxiety and depression. Long-term consequences of wearing facemask can cause health deterioration, developing and progression of chronic diseases and premature death. Governments, policy makers and health organizations should utilize prosper and scientific evidence-based approach with respect to wearing facemasks, when the latter is considered as preventive intervention for public health."
On 2021-05-28 12:53:12, user rusbowden wrote:
Earlier, I pointed out that the study does not show that mask use fails to protect the individual, mostly looking at more meta data about mask mandates versus virus spread. It's simply not what the study is about. It is about the effectiveness of mandates. The data the researchers used for mask use comes from Washington IMHE, which urges mask use. And here I will point that the researchers seem to be outside their areas of expertise. This study also supports the idea that masks cause delays in upswings, which may mean that contracting the virus took place more while unmasked. We cannot make the leap to say that wearing a mask does not help the individual. It is irresponsible to do so.
There's a further problem with the robustness of this study, which goes beyond simple timing and groupings. It has to do with not holding other factors constant. For instance, did mask use cause people to breach social distancing guidelines, and how much enforcement was used in different states. There's a tale of 2 cities here in Massachusetts, Lowell, which was lax in enforcement and attitudes, and Cambridge, which levied fines. When you entered Cambridge, you see most people wearing masks -- especially during the day -- not so in Lowell. Surreptitious unmasking did take place at night in Cambridge, especially among men (who should be wearing masks if for no other reason then to make others feel safe around them -- another psych/social, which were not allowed discussed). But, Cambridge, a more congested city of the same population size, had less cases per population than Lowell -- which as I mentioned earlier only got off the high-risk level a couple weeks ago.
On 2021-05-27 18:54:42, user alejandro wrote:
Maybe this is interesting for you https://www.biorxiv.org/con...
On 2021-05-28 00:56:34, user Jian Zhang wrote:
According to Figure 2B, there is clearly a two- to three-fold increase of anti-Syncytin-1 after vaccination (especially 1-4d and 6-7w) compared to Day 0.
On 2021-05-31 06:51:28, user Luca Prosperini wrote:
Where is the TABLE 1?<br /> Thank you
On 2021-06-02 08:09:56, user Le Bon wrote:
The idea of looking at patients who had at least a substantial cumulated dose is great, but there is an important immortal time bias, since the patients can't die the first 10 days in the HCQ group, as seen on the Kaplan-Meïer
I suggest to calculate again the results with excluding the first 10 days death in the control group.
Due to the small group size, you will probably loose significance, but it still will be usefull for pooled analysis.
On 2021-06-09 16:25:49, user livefreeinTX wrote:
It's heartbreaking to me that all those hundreds, perhaps thousands, of NYC patients in the spring of 2020 were left to sit around at home until they could barely breath and were then hospitalized and put on ventilators, and were denied HCQ, which may have saved hundreds of lives. Truly sickening, imo.
On 2021-06-10 04:44:14, user John Jay wrote:
Sorry if I missed it, but was there a discussion of how the demographics (ie age, co-morbidities, status before treatment, etc.) differed or didn’t differ between the 3,000mg HCQ + 1,000 AZM group and the rest of the patients?
On 2021-06-02 17:51:00, user Jørgen K. Kanters wrote:
The paper has now been accepted and published in Scientific Reports 11(1) 1-11 (2021)
On 2021-06-03 18:02:57, user Peter Ellis wrote:
"We conclude that it is almost certain that there is increased transmissibility that will rapidly lead to B.1.617.2 becoming the prevailing variant in the UK."
This was posted on the day Public Health England released a report showing that the Delta variant (B.1.617.2) is currently 73% of sequenced cases - i.e. it was 73% of new cases a couple of weeks ago. S gene proxy data is only a week out of date and has the prevalence of Delta at 85.4%
Forget journals not being able to keep up, even preprints can't keep up with this.
On 2021-06-08 03:53:14, user Emma Tan wrote:
What is the PPA and NPA if a PRNT cut -off of 1:20 is used instead (1:20 is recommended as positive result)?
On 2021-06-09 16:22:28, user Vojtech Huser wrote:
Great paper about a tool that is used by OHDSI researchers.<br /> Relationship to Achilles Heel prior tool would be a good added discussion. Contribution from the community to the tool (besides core authors) can also be described.
On 2021-06-11 15:37:05, user Bob Leon wrote:
Below is an excerpt from the full text stating that the purpose of the study was to prove that it was beneficial for the previously infected to still receive the vaccine. Thankfully the researchers had the ethics to report that they found the opposite of what they purposed to find.
"A strong case for vaccinating previously infected persons can be made if it can be shown that previously infected persons who are vaccinated have a lower incidence of COVID-19 than previously infected persons who did not receive the vaccine.
The purpose of this study was to attempt to do just that,"
On 2021-12-30 11:33:49, user Suruchi wrote:
CORRECTION: The crude seroprevalence was 89.5% (95% CI 89.1, 89.8).
Dr. Suruchi Mishra
On 2021-06-14 03:42:27, user Jones Onigbinde wrote:
Hi. Great work. I do however have an issue with the way you injected political dichotomy into the COVID-19 outlook. In your DAG diagram you inferred that having a right wing populist idea somehow contribute to the spread of the disease but you do not mention the radical left wing rioting that occurred all around the world in the summer of 2020. You forgot that people who are right leaning are more likely to believe that the virus actually came out of a Wuhan lab which left leaning media, scientists, and politicians termed to be a conspiracy theory for the past one year. Now the theory is becoming more and more plausible. My advise is that you should keep politics out of science. Follow the evidence wherever it may leads, that's science. It appears to me that 2020 was the year science came to die because of the propensity of people like you to tailor science to politics.
On 2021-06-17 16:13:50, user Hao Yin wrote:
Note: Contents in this draft are our preliminary results. The final results of this study are published on the journal, Lancet Planetary Health, please check out our online peer reviewed paper: https://doi.org/10.1016/S25...
On 2021-06-18 23:08:13, user Number Six wrote:
A question on the definition of "infectious" people in your model.
Are you using positive test results and defining those as infectious people?
On 2021-06-22 15:51:27, user Amit Kumar wrote:
The paper has been published in a peer-reviewed journal Aerosol and Air Quality Research with the following DOI number.<br /> https://aaqr.org/articles/a...
On 2021-03-22 13:21:54, user Stephen B. Strum wrote:
The Gorial et al. study in my opinion is a weakly positive study re ivermectin. The IVM group had 25% of patients with co-morbidities vs 45% in the non-IVM group. Gorial's reference 14 is a retracted paper (Patel). Positive findings re IVM were shorter times ot – PCR with 7 days for IVM vs 12 for non-IVM. Mean hospital days 42% less in IVM arm. I wish Gorial would have detailed the 2 fatalities in the non-IVM arm. Someone should have proofed this paper; it is very sloppily written. In contrast, the paper by Krolewiecki et al. is very impressive re IVM & the importance of pharmacokinetics.
On 2021-03-24 09:22:16, user Sarwah Al-Khalidi wrote:
This paper fills an essential gap by surveying the hesitancy rates of being vaccinated against the COVID-19 virus among Arab-speaking individuals, and investigating associated hesitancy factors. It is the first study of this scale in the Arab world, with over 36 thousand individuals from all 23 Arab countries and beyond.
The multidimensionality and the well-thought out plan of both the survey and the analysis are truly impressive. The use of 29 objective points to measure the level of Hesitancy gives this paper great power. The importance of this study is evident form results that indicate that 60% of the Arab population are hesitant to take the vaccine. This is a striking percentage to anyone fighting against this pandemic. Using multivariate analysis to deconvolute key factors effecting hesitancy makes results more comprehendible. Interestingly, results of the multivariate analysis show that people typically classified as high-risk (above 60 or have a chronic illness) are the least hesitant to take the vaccine, which could be reflective of the media and government’s influence on people’s decision.
Among the tested factors that could be affecting a person’s attitude, the frequency of taking the flu vaccine seems most convincing, and could be indicative of a person’s confidence or knowledge about vaccines. It is surprising that the hesitancy among health workers is not significantly less than that of those who don’t work in the health system.
By revealing the main barriers to taking the vaccine against COVID-19, results published in this paper are an essential step forward towards tackling the pandemic in the Arab world.
On 2021-03-24 12:15:54, user Rogerblack wrote:
This studies depression and anxiety measure ASSUMES A HEALTHY PATIENT. 'little energy', 'trouble concentrating' 'moving slowly' = a minimum score of 3 due to physical symptoms of longcovid/fatigue. If very exhausted, this can easily rise into the 'severely depressed' range.
It is not unreasonable to use the PHQ-9 or similar as a screening measure of disease severity.
To use it in a patient population suffering from fatigue, concentration problems, ... is guaranteed to cross-read between those symptoms and anxiety - it is useless without a careful assessment of each question to find if you are measuring MH, or physical symptoms.
It absolutely cannot justify sentances such as "The physical, cognitive and mental health burden experienced by COVID-19 survivors was considerable. This included symptoms of anxiety and depression in a quarter" without much more work, as it will lead to the conclusion that treating depression may benefit the patient when there is no depression, and it's a scale artifact.
PHQ9 and similar scales are designed for patients without significant physical comorbidities to the mental state they are trying to measure. The normal scale cuts are only valid for this purpose.
I note similar concerns to those raised with the C-MORE paper. (https://www.medrxiv.org/con...
Edit: response to the promoter account on twitter in July raising this issue.
https://twitter.com/SithEle...<br /> '@PHOSP_COVID<br /> What is the current analysis plan and instruments (BDI,SF36) planned to be used to measure health? I am concerned that instruments can be misinterpreted and cross react between physical and mental health.'
On 2021-03-24 15:30:41, user Stephen B. Strum wrote:
I am puzzled. The full article I found with the exact same title is different from the article found on this website. The abstracts are not the same. Here's the conclusion from the pdf I found before finding this site with the exact same title and authors:
"Conclusion: The results of our target trial emulation match with previous findings of randomized clinical trials and observational studies, which showed no beneficial effects of hydroxychloroquine, ivermectin, azithromycin, or their combinations."
Compare the above with the conclusions found on this site:
"Conclusions Our study reported no beneficial effects of hydroxychloroquine, ivermectin, azithromycin. The HCQ+AZIT treatment seems to increase risk for all-cause death."
Why is there this dicrepancy?
On 2021-03-29 19:49:55, user killshot wrote:
This paper needs major review. Statins do not "improve endothelial function". If anything they are anti-inflammatory. Also there is very little discussion of randomization. If the group is not randomized minimally with vitamin D levels, the whole study is meaningless.
On 2021-04-09 01:46:20, user Yq Zhang wrote:
Is it possible to make the data public in addition to the code?
On 2021-04-10 11:14:32, user John Smith wrote:
I have been following your studies and find it fascinating, you've done an excellent job. Would be interesting to see Turkey's figures due to their rapidly rising infection rate. I see on the Economist/NYT websites they only have Istanbul figures with an undercount ration of 1.55. Is it possible to obtain the whole country's figures do you think?
It's a shame that a lot of people look to the Worldometer site for their figures when so much of the information is incorrect/incomplete. It would be a great idea if they had a separate column showing 'total deaths including excess mortality' next to the 'total deaths' column to show a truer picture.
On 2021-05-12 13:15:26, user John Smith wrote:
Hi, I see the IHME have just published their excess death figures:
http://www.healthdata.org/s...
I was wondering how they came to their figures on Japan and Kazakhstan which differ from yours substantially.<br /> They have Japan as 108,320 excess deaths and Kazakhstan as 81,696. They also differ with many others also. Interesting reading.
On 2021-04-12 14:22:11, user Okan Bulut wrote:
Our study has been accepted for publication in the Journal of Mixed Methods Research. Please see the full citation, including the title change for our study below:
Poth, C., Bulut, O., Aquilina, A., & Otto, S. (In press). Using data mining for rapid complex case study descriptions: Example of public health briefings during the onset of the COVID-19 pandemic. Journal of Mixed Methods Research.
On 2021-04-13 07:54:42, user helene banoun wrote:
Infections within 14 days of vaccination are not taken into account: experts have warned that ADE can occur in the first few days when vaccine antibodies are at low levels and low affinity
Why were people tested in PCR? were they control PCRs, were they sick, hospitalized?
The maximum Ct to consider a positive PCR is set at 33, it has been published that from 28-30 no live virus can be cultured: why not choose this threshold?
The matching may have led to the elimination of people carrying virus fragments because their Ct was higher than 33.
On 2021-04-16 12:52:13, user bluenoser2 wrote:
Peer reviews of the study are now available at Rapid Reviews: COVID-19 https://rapidreviewscovid19...
On 2021-04-14 08:04:37, user Muhammad Yousuf wrote:
Implications of SIREN Study regarding immunity and reinfection after documented SARS-CoV-2 infection
According to this study (1) done in the UK in Health Care Workers (HCWs), the cohort having evidence of previous documented SARS-CoV-2 infection had the following observations:<br /> 1. The immunity was noted up to 7 months after the incident COVID-19 infection<br /> 2. 155 infections were detected in the baseline positive cohort of 8278 participants (1.87%).<br /> 3. The cohort with past COVID-19 after reinfection were mainly asymptomatic or had milder symptoms with no mortality.<br /> This augurs well regarding immunity in most people who have recovered from COVID-19. Immunity may last for over 7 months (more follow up of this cohort will be more informative to assess the long-term immunity. However, most of such HCWs were female and younger. The immunity duration after SARS-CoV-2 infection will need more such studies in people >65 years particularly in males who are mainly being affected by COVID-19 pandemic.
On 2021-04-15 11:01:12, user Ian Viney wrote:
Interesting paper, and although an approximation I think it makes a good point. Having conducted similar studies to reconstruct research income, I share the methodological frustration that funders do not always provide basic financial details for awards (exceptions include UKRI, Wellcome, NIH and many others), institutions do not always provide details of the research projects they secure (exceptions include Kings College London, Edinburgh University and many others), publishers don't capture structured authoritative grant information in their articles (despite the efforts of FundRef etc.), and authenticated information cannot be easily re-used/compiled (despite the efforts of ORCID). As a result there are clearly a lot of investments that your study is missing. One element is the support that Oxford and other UK and international institutions will have provided to the work. The financial details for the grants you have identified will in the main be the amounts awarded by the funder, not the full economic costs of the work. Your FOI might have been an opportunity for you to collect the full cost of each project, and I'm surprised that Oxford didn't comment on this. As most government funded grants are awarded on the basis of 80% of full-economic costs, the institutional contribution may have been ranked third in your analysis. Of course the institutional contribution to the work will be supported from a variety of sources with one major element being the UK funding council grant, so also substantively publicly funded. This would therefore have not have changed your overall conclusion. Some nice context to the public and charity funding for UK health research, with an overall estimate of the contribution from various sectors can be found in the recent UKCRC report at www.hrcsonline.net.
On 2021-04-19 11:59:37, user lotrus28 wrote:
Has this study been submitted to a journal?
On 2021-04-20 16:21:52, user Laurie B wrote:
Thank you for conducting this important research work and making your results available online. This information must be widely communicated. My dad received his final Retuxin infusion January 2021. Shortly after he received Covid vaccination 1 and then February 4th the second. While still following most covid precautions he had certainly let his guard down as a "fully vaccinated" person. Turns out, he was not. He is in the ICU with covid. Please pursue a press release. Please let me know how I can help disseminate your findings. Thank you for your work!
This is how our family found out: https://www.nytimes.com/202...
And from an ICU Doc who shared: "Rituximab specifically target cancerous B cells and helps our immune system destroy them. But B cells are the very cells that make our antibodies so his response to the vaccine is going to be muted with or without the Rituximab."
On 2021-04-21 15:08:18, user Rafael wrote:
Interesting work. We also found Prevotella sp. associated with COVID-19 severity in https://www.frontiersin.org...
On 2021-04-26 00:57:11, user jgas wrote:
Intrigued by the 1-21 days pre-vaccination data.<br /> If the 5% of total positive PCR in the 21 days pre-vaccination (compared to 85% occurring in those more than 21 days pre-) is just down to people increasing behavioural shielding -extra NPI caution because "daft if I get Covid19 now when I'm so close to getting protection", what explains the reduction in self-reported 'typical Covid19 symptoms' i.e cough/fever/anosmia in the positives from this same period?<br /> If extra caution -> lower rate of positives and also less symptomatic positives is this mediated by scant innoculum?<br /> How does the timing of the big post-Christmas wave and ensuing lockdown interact with these data?
On 2021-04-26 13:56:45, user Zorak wrote:
2 deaths in 200 cases. As far as we know, it is the same ratio of "untreated" cases. There's no improvement with this treatment.
On 2021-04-27 05:35:58, user SSS wrote:
Ok so there are at least 100 articles showing vaccines cause thrombosis. you can start by looking at the references in this article. youre welcome. https://www.ncbi.nlm.nih.go...
On 2021-04-27 19:49:26, user louiea wrote:
The assumption: "we assume constant mask filtration pm over the entire range of aerosol drop sizes." is a bad assumption and supported by the referenced papers. Optimal mask efficiency can only be achieved with N95 masks that are properly worn (no gaps), All other masks types have filtration efficiencies around 50% or less. (ref 69).
On 2021-04-30 11:11:21, user Kontrolletti wrote:
I am surprised by some of the numbers in the Introduction section, specifically "...the cumulative hospitalization rate has exceeded 1300 persons per 100,000 since early 2020 (2). Hospitalized patients account for 1% of COVID-19 patients...".
Today the source given for the cumulative hospitalization rate gives a number of 531.5 persons per 100.000 for the week ending April 24. Also today, the CDC report a number of roughly 32 million total cases reported and a number of 2.1 million total new hospitalizations, which would mean that hospitalized patients would account for 6.5% of COVID-19 patients (https://www.cdc.gov/coronav... "https://www.cdc.gov/coronavirus/2019-ncov/covid-data/covidview/index.html)").
On 2021-05-04 16:08:58, user Don Lotter wrote:
Could much of COVID vaccination resistance be due to the person having had the virus & belief that they are immune?<br /> What portion of that vaccine hesitant 30% are people who have had the coronavirus and, quite justifiably ( https://www.nature.com/arti... "https://www.nature.com/articles/s41590-021-00923-3)"), feel that they are already immune and don't need the shot? Why isn't this question being asked? Because it is an important one in the herd immunity calculation.<br /> And yes, I realize that there are no hard stats on previous infections, but an estimation could at least be made based on studies. It might pull the 30% down to, say, 20%, that 20% being those who were<br /> likely never infected and yet are hesitant. It would push the total immune percentage up in the herd immunity quest.
On 2021-05-07 16:36:27, user Gustavo wrote:
It would be very interesting if the researchers compared the levels of vitamin D (25OHD) in the two sisters. Vitamin D is actually a hormone with an immunomodulatory effect. A 2010 survey identified that sufficient levels of vitamin D are crucial for the activation of CD8 + killer T lymphocytes:
https://www.sciencedaily.co...<br /> von Essen et al. Vitamin D controls T cell antigen receptor signaling and activation of human T cells. Nature Immunology, 2010; DOI: http://dx.doi.org/10.1038/n...
This finding was confirmed by these two recent studies:
-Circulating Vitamin D levels status and clinical prognostic indices in COVID-19 patients<br /> https://t.co/FpTJ0vwWkc
-The association between vitamin D levels and the clinical severity and inflammation markers in pediatric COVID-19 patients: single-center experience from a pandemic hospital
On 2021-05-08 08:06:03, user Dennis Kleid wrote:
It seems to me that the model needs to take into account what folks are doing in that room. In a restaurant or a nice dinner party, people are eating, talking, laughing, and having fun over their meals. No masks, lots of aerosols; let's say just one person is sick.
The issue is: "In the presence of a quiescent ambient, they (e.g. the particles with virus), then settle to the floor". In this room, much of the exposed "floor" is interrupted by everyone's plate or food. The virus will enjoy the landing and stay for a while.
"Hey, Uncle Joe [Namath/Montana, at the other end of the table], please pass the spaghetti". Infection via the mouth needs to be considered. Airborne transmission?
On 2021-05-08 20:45:10, user greenorange041 wrote:
This is a very thorough analysis indeed. But I think it is extremely dangerous just to assume that all excess mortality is due to the COVID infection (and you do exactly this if I got it right). It may well be indirectly caused by COVID, but in fact be a more direct consequence of various restrictions imposed by governments and reduced economic activity.
When people lose jobs or their business becomes effectively banned, they do not necessarily expect to die from hunger immediately. But when usual sources of income become unavailable, it puts people under strong pressure and can quickly cause psychological problems that may make them vulnerable to other diseases and in the worst case can lead to suicides. This is especially true when the situation of high uncertainty persists over months without much hope of returning to normality quickly. And this is the moment when the risk of dying from hunger gets higher.
This is also why poorer nations are in general much more affected because their population has less savings on average and is often dependent on richer nations because this is where a considerable amount of their citizens work, including the industries affected by the restrictions (and richer countries could afford especially strict lockdowns). Even if they work in other sectors, travelling between countries became more cumbersome, which is why some of those people had to stay in their home countries having no clear prospects of finding work.
You account for none of these factors. Arguably, it is difficult, but to separate the negative effect that COVID itself has caused from the negative effect all government measures have caused is absolutely necessary for a meaningful analysis.
On 2021-05-10 09:54:41, user Auroskanda Vepari wrote:
Do the findings suggest that patients who suffered a natural infection resulting in detectable anti-spike antibodies do not necessarily require a single or double does of a vaccine?
On 2021-05-12 14:25:32, user Remi Goupil wrote:
This preprint is now published with updated data in CMAJ at https://www.cmaj.ca/content...
On 2021-05-14 01:56:12, user J.A. wrote:
In reviewing Tom Argoaic comment, I looked at the public dataset. In the dataset, the days from exposure to starting study drug or placebo are listed as 1 to 6 days. In the preprint tables 1 and 2, there are none listed for 1 day and 28 people listed for 7 days. It seems very clear that the authors of the preprint have altered the data. There is nothing in the methods explains that the data were altered. It looks like the authors chose to inflate the delay from exposure to starting medicine by +1 days for everyone. As this time from exposure to starting the study medicine is the primary focus of the preprint, this should be clear to readers and should be correct. Furthermore, not altering the data would seem to yield the same statistical analysis, yet have the benefit of being correct. This should be corrected.
Second, the authors should consider making a figure to visually show what the authors are trying to present. While there are many tables, visually showing the percentage with COVID-19 by day 1-6 would be a better way to present the data, with the mean +/- 95 confidence interval for the estimate.
Third, the authors should discuss why the placebo event rate varies over time. The placebo event rate is 10%, 15%, 19%, 12%, 13%, and 0% over the day 1-6, is there a biological reason for this variation or this random variation? The day 3 group has the highest event rate (18.9%), which then makes the statistical difference. Is this an artifact or is there biological plausibility for why taking placebo on day 2 or 4 is much better than day 3. Perhaps add this to the discussion to explain why this is not all just a post-hoc artifact of small subgroups.
On 2021-09-15 14:55:00, user Donald Milton, MD, DrPH wrote:
This manuscript was accepted by Clinical Infectious Diseases and published online on 15 September 2021. https://academic.oup.com/ci...
On 2021-09-17 21:12:27, user Jeff wrote:
The denominator for the number of vaccinations seems wrong. The paper says "we recorded all vaccinations given in the Ottawa area between 1st June and 31st July 2021," and "there were 15,997 doses of Moderna vaccine, and 16,382 doses of Pfizer vaccine administered over the study period, for a total of 32,379 doses". But this seems like a gross undercount. On the Ottawa public health vaccine dashboard (https://www.ottawapublichea... "https://www.ottawapublichealth.ca/en/reports-research-and-statistics/COVID-19_Vaccination_Dashboard.aspx)"), the chart showing doses administered per week <br /> suggests that over 800,000 mRNA vaccine doses were administered in this time period. Were other criteria applied to reduce the denominator, or is this an error?
On 2021-09-25 16:30:29, user TeeJay2000 wrote:
I left a comment reflecting on the reputation hit that the Ottawa Heart Institute will take on this, but my comment was removed. Thank you medRxiv for encouraging discussion. I have now written to the Ottawa Heart Foundation, to indicate my withdrawal of support, until the Institute makes a formal statement how this paper made it even to a 'preprint', given the colossal size of the error.
On 2021-09-19 11:26:29, user Day Evenson wrote:
Is there any study that separates the unvaccinated into those who have had Covid and those who have not? I can't find any research on vaccinated vs previously infected. What is the lasting immunity between these groups?
On 2021-09-20 13:55:05, user mike marchywka wrote:
There is a lot tto be learned from the aging issues,
On 2021-09-21 04:34:22, user Shawn Mclean wrote:
Wheres the raw data for this survey? It would be great if it's made public so we can dig into it ourselves.
On 2021-10-20 01:13:14, user rferrisx wrote:
The PHD hesitant numbers were adjusted for v2?:<br /> https://www.medrxiv.org/con...<br /> Page 24 table PHD:<br /> 23.9 (22.7, 25.1)v1<br /> 14.6 (13.5, 15.6)v2
On 2021-09-21 09:06:34, user Muhammad Yousuf wrote:
Notwithstanding the comments this preprint is generating, it would also be interesting to compare three groups in this study with another group who were COVID-19-naive but received 3 doses of Pfizer's vaccine including a booster dose. If the immunity and protection against SARS-CoV-2 is still higher in infected plus vaccinated compared with those having three doses of COVID-19 vaccine, this will indicate that there is immune memory (1) through bone marrow plasma cells at play.
On 2021-10-15 12:41:54, user Mithat Temizer wrote:
Here is the question. Age is being treated in all models as a potential confounder. For a confounder age needs to be associated with COVID-19 outcome regardless of vaccination status AND age should be associated with vaccinations status regardless of COVID-19 infection. Both assumptions can be considered fulfilled in the model. Yet, the third assumption that age is not on the pathway between vaccination status and the COVID-19 infection/complication (such as hospitalization/death). In this case, we cannot confirm that age is not in the pathway. That is age is not a confounder. Could be an intermediate variable or more likely an effect modifier for the vaccine-induced/native infection-induced immunity against COVID-19 infection. In this case, why is age not considered in analyses as an effect modifier? I wonder whether the authors have checked for the effect size of vaccination (compared to natural immunity) in any of the 3 models, stratifying on age (such as those below 60 years versus those aged 60 years or more). Any comment on this?
On 2021-10-21 02:21:14, user JWrenn wrote:
A few odd things with this study.<br /> 1. why wasn't a control group of infection rates /hospitalizations of unvaccinated and never had covid included? <br /> 2. why wasn't a control made for behavior difference?
Seems like the numbers rates they put forward are not a great number to base this all on. Instead we should be looking at difference between totally unimmunized and immunized via vaccination and unimmunized and immunized via infection. Otherwise the numbers come out so tiny that it gets very weird...ie 1 vs 8 out 32k really is almost so small that it becomes random.
However if say 1000 would have been sick with no intervention then you get better numbers. like 1000-1=999 less vs 1000-8=992 less and you can see that both are very effective, but one is more so.
Also, the 2nd point really kind of breaks the whole thing. In my experience people who had Covid (and were not asymptomatic) are far more careful than people who have not gone through that hell.
The info is good just seems incomplete, and that behavior aspect I think is fare more important that we are wanting to admit as well as hard to account for in database studies.
On 2021-09-22 19:56:45, user Steve E wrote:
Unfortunately, even your high-vaccination-hesitancy-level scenario, which leads to national vaccination coverage saturation at 70%, now seems too optimistic. Today's CDC vaccination data shows we may not even reach 60% by year's end (unless the Biden mandates change the situation dramatically). How do your projections change in a 60% scenario?
On 2021-09-24 20:53:59, user Kenny wrote:
Very surprised that there is no evidence of lowering total mortality. Essentially there is absolutely no direct evidence that vaccine saves life.
On 2021-09-28 12:29:12, user Azmeraw Ambachew Kebede wrote:
This paper has been published at PLOS ONE (https://doi.org/10.1371/jou... "https://doi.org/10.1371/journal.pone.0255021)")
On 2021-09-29 06:49:42, user Amador Goodridge wrote:
Excellent article. Looking at mask use behavior remains key to acknowledge the human being response for this and any future repiratory pandemic. Fernandez-Marin and his co-authors highligth the variations of mask use behavior. I agree that special attention should be directed to suburban areas, where social determinants for public health are sustaining the transmision of COVID-19 and many other infectious diseases. Congratulations to the authors!
On 2021-09-29 11:57:21, user kdrl nakle wrote:
Awesome, confirms what I have always suspected and it relates well to earlier research into European intro of SARS-CoV-2 (5-6 R0).
On 2021-09-30 10:22:03, user V Deepak Bamola wrote:
This preprint is under review at 'Experimental Biology and Medicine'<br /> @medrxivpreprint:Effect of Bacillus coagulans Unique IS-2 in Inflammatory Bowel Disease (IBD): A Randomized Controlled Trial https://t.co/hH32BrOdYT #medRxiv
On 2021-10-01 11:24:21, user Mahalul Azam wrote:
This work now published in the Int. J. Environ. Res. Public Health with the DOI https://doi.org/10.3390/ije...
On 2021-10-01 21:43:06, user Frank Jones wrote:
This study is deeply flawed as it relies on PCR. The PCR tests do not perform melting curve analysis to identify false positives due to primer dimers or other unspecific products. This is especially a problem if the target template concentration is low or if over 30 cycles are performed. I did thousands of quantitative PCRs and yet have to come across a primer pair that does never produce unspecific signal at high cycle numbers. This process is stochastic due to the nature of primer annealing, so a sample can be false positive or negative when running it multiple times under identical conditions which explains why some patients test positive and the next day they are negative. Also, there is no appropriate control to identify false positives. The no-template negative control is not sufficient since it obviously cannot prove the primers or probes do not amplify off target templates. Only the sample of a confirmed Covid negative person would be acceptable, yet this is not done.
On 2021-10-16 11:51:18, user vAsisTha wrote:
Explains why highly vaccinated countries still have high covid+ve rates
On 2021-10-03 05:25:47, user kdrl nakle wrote:
Put the dates in abstract or in title. June 2020 for this serosurvey. Quite irrelevant now, more than a year after, good only for historical reference.
On 2021-10-03 09:35:28, user kdrl nakle wrote:
Nothing new in this paper.
On 2021-10-03 11:19:07, user kdrl nakle wrote:
You could call this "Large University in a Large Town". These titles are really ridiculous. Can't you just write USC? <br /> Another thing, faculty over the age 52 are 3.4 times more likely to be unvaccinated than those in age group 20-32? That does not make sense to me.
On 2021-10-04 06:59:17, user kdrl nakle wrote:
EMT, does not surprise me. Too bad this is before Delta.
On 2021-10-06 08:55:05, user Ken wrote:
at the time being, working on an update, we found that the spirals work even better if you sobsitute the number of infected witrh the number of infected per 100.000 inhabitants.<br /> Using the incidence could help with the calculations by simplifying the 0 pahse
On 2021-10-10 05:22:31, user kdrl nakle wrote:
I'll keep this paper in mind, it really looks realistic but so far most of COVID projections turned out completely wrong.
On 2021-10-10 05:35:31, user kdrl nakle wrote:
I am sorry but this is example of a poor research. "We suspect Delta variant"? Couldn't you find that out? "The infection does not spread (much) thoughout body"? Really? What does "much" mean here?
On 2021-10-11 18:46:13, user Andrew T Levin wrote:
Given the stated purpose of this study, it is remarkable that the manuscript never specifically defines the term “community-dwelling population.” In practice, the study analyzes the incidence of COVID-19 fatalities that have occurred outside of nursing homes, but even that distinction is not very precise. For example, the spectrum of U.S. nursing homes encompasses board & care homes, assisted care facilities, and skilled nursing facilities. About two-thirds of U.S. nursing home residents rely on Medicaid to cover that cost. By contrast, higher-income individuals can afford to receive home health care or choose to live in “retirement communities” with on-site medical staff. In effect, the distinction of whether someone is “community-dwelling” or a “nursing home resident” is linked to a complex set of socioeconomic characteristics as well as to various aspects of their individual health. Making international comparisons along these lines is even more fraught with difficulty, because the size and composition of the nursing home population inevitably reflects differences in social norms as well as socioeconomic factors, access to healthcare, and the extent of public assistance. Indeed, such comparisons may be practically meaningless when considering developing countries such as the Dominican Republic and India, where nursing home care may only be an option for a very small fraction of the population.
Search Procedure. This manuscript uses an arbitrary search cutoff date of 31 March 2021, which excludes some landmark seroprevalence studies that have been disseminated since then. For example, Sullivan et al. (2021) analyzed seroprevalence of the U.S. population over the second half of 2020 using a large representative sample that included 1154 adults ages 65+, and hence that study would clearly satisfy the stated eligibilitry criteria for this meta-analysis.[11] Moreover, the study carefully adjusts for assay characteristics and seroreversion and estimates that as of 31 October 2020, the IFR for U.S. adults ages 65+ was 7·1% (CI: 5·0¬-10·4%). Those results can be also be used in conjunction with data on nursing home deaths to obtain the corresponding IFR estimate of 4·7% for community-dwelling adults ages 65+.
Minimum Size Threshold. This analysis excludes seroprevalence results from any studies involving fewer than 1000 adults ages 70+, and hence it is remarkable that the manuscript neither provides any rationale for imposing such a constraint nor provides citations to any existing works that might motivate it. Indeed, this approach is inconsistent with basic principles of statistical analysis, e.g., making inferences based on all available information and avoiding arbitrary selection criteria that could induce bias in the results. Consequently, meta-analysis should downweight studies with relatively lower precision rather than simply discarding those studies. Moreover, it is incoherent to specify an eligibility criterion based solely on sample size, because the precision of seroprevalence estimates also hinges on the level of prevalence. A small sample may be adequate in a context of relatively high prevalence, whereas a much larger sample may be needed to obtain precise inferences in a context of very low prevalence. The national study of Hungary was included in this meta-analysis because that study included 1454 adults ages 70+. However, only nine of those individuals were seropositive. Consequently, the test-adjusted seroprevalence for this cohort of older adults is not statistically distinguishable from zero, and hence the confidence interval of the age-specific IFR is not even well-defined.[12] By contrast, the regional study of Geneva was excluded from this meta-analysis because it only included 369 individuals ages 65+. But that sample was large enough to facilitate inferences about seroprevalence (6·8%; CI: 3·8¬¬ 10·5%) and corresponding inferences regarding IFR for that age cohort (5·6%: CI: 4·3 7·4%).[13, 14] Finally, setting the sample size threshold at 1000 is clearly an arbitrary choice. Since seroprevalence studies can be readily identified using the SeroTracker tool, this meta-analysis should be extended using a lower threshold of 250 adults ages 65+ that would encompass the national studies of Netherlands and Sweden as well as a substantial number of regional studies.
Sample Selection. In characterizing which seroprevalence studies have been included in <br /> the meta-analysis, this manuscript specifies the key criterion as “aimed to generate samples reflecting the general population.” However, this criterion is extraordinarily vague and judgmental (as evident from subjective words like “aimed” and “reflecting”). <br /> (a) United Kingdom. The inadequacy of this approach to sample selection is evident from the fact that the meta-analysis places equal weight on four U.K. seroprevalence studies, even though only two of those studies (UK BioBank and REACT-2) utilized samples designed to be representative of the general population.[15, 16] By contrast, the other two studies used convenience samples that were not designed or even re-weighted to be broadly representative, and hence those two studies should have been excluded from this meta-analysis. First, Hughes et al. (2020) studied a panel of primary and secondary patients at a large Scottish health board, with the stated objective of assessing viral transmission patterns.[17] The paper never suggested that this panel could be interpreted as representative of the wider population; indeed, some of these patients may have been receiving care related to COVID-19. Second, in one of its weekly surveillance reports, Public Health England (2020) reported seroprevalence results for a panel of patients ages 65+ who had a routine blood test at the Royal College of General Practioners Research and Surveillance Centre.[18] Evidently, this panel was not aimed to reflect the general population and may well have included patients recovering from COVID or experiencing COVID-like symptoms. <br /> (b) United States. One of the two U.S. seroprevalence studies used a sampling design that is intended to be broadly representative, whereas the other U.S. study used a convenience sample of patients at kidney dialysis centers. Unfortunately, as a consequence of gross disparities in healthcare access, higher-income individuals typically utilize in-home dialysis machines, whereas low-income individuals must travel multiple times per week to a dialysis center, often using public transit. Consequently, the prevalence of COVID-19 infections among such patients has crucial public health implications but should not be interpreted as representative of the general population.<br /> (c) Canada. Among the three Canadian seroprevalence studies, two use representative sampling designs (Ontario and Canada-ABC), whereas the third study conducted by Canadian Blood Services (CBS) uses a convenience sample of blood donors. In its public announcement of those results, CBS specifically warned that “caution should be exercised in extrapolating findings to all healthy adult Canadians, because blood donors self-select to be blood donors, in some areas access to a donation clinic may be limited, and there are fewer elderly donors who donate blood compared to the general population.” [19] That caution was specifically cited as the reason for excluding this study from a previous meta-analysis.[5] Indeed, given the scarcity of elderly blood donors, there is an even stronger rationale for excluding that study from the analysis here. Indeed, this meta-analysis should have specifically excluded all convenience samples, whether from blood donors, commercial lab tests, or medical patients. Dodd et al. (2020) analyzed a large panel of U.S. blood donors and found that the proportion of first-time donors jumped in June 2020 following the introduction of COVID-19 antibody testing, consistent with the hypothesis of “donors with higher rates of prior exposure donating to obtain antibody test results,” and concluded that “blood donors are not representative of the general population.”[20] Bajema et al. (2021) found seroprevalence of 4·94% using commercial lab residual sera from residents of Atlanta (USA), compared to seroprevalence of 3·2% using a representative sample of the same location.[21, 22] These findings highlight the extent to which convenience samples may be associated with upward bias in seroprevalence and hence downward bias in IFR. It should also be noted that the incidence of COVID-19 infections has a strong association with race and ethnicity, reflecting disparities in employment, residential arrrangements, and various other factors. Such patterns have been evident in numerous countries (not just the USA), and hence the manuscript should follow a consistent approach in addressing this issue.
Open-Ended Age Brackets. This manuscript proceeds on the assumption that open-ended age brackets for older adults are essentially equivalent regardless of whether the bracket is 60+, 65+, or 70+. But this assumption is inconsistent with the consistent findings of preceding studies, namely, the IFR for COVID-19 increases continuously with age rather than jumping discretely at any specific age threshold. Indeed, the measured IFR for any particular age bracket is a convolution of the age distribution of the population, the age-specific pattern of prevalence, and the fact that IFR increases exponentially with age. The complexity of this convolution underscores the pitfalls of comparing IFRs for open-ended age brackets of older adults. Ontario serves as a useful case study for illustrating these issues. The Ontario Public Health seroprevalence study reported results for three broad age brackets: 0-19, 20-59, and 60+ years. However, this manuscript assesses IFR for ages 70+ using results obtained via private correspondence. However, that assessment may be very imprecise, because COVID-19 prevalence was very low in the general population and may well have been even lower among the oldest community-dwelling adults. By contrast, the Ontario study is very informative for characterizing the cohort of individuals ages 60-69 years. In particular, there were 9 positives among 804 specimens for that cohort; the test-adjusted prevalence of about 1% indicates that about 17000 Ontario residents ages 60-69 had been infected by mid-June 2020. As of 30 June 2020, that age group had 240 COVID-19 deaths—none of which occurred in nursing homes. Consequently, the IFR for community-dwelling Ontario adults ages 60-69 was 1·4% -- identical to the predicted IFR t the midpoint of this age interval from the metaregression of Levin et al. (2020).[5]
Adjusting for Assay Characteristics. Seroprevalence studies have generally been conducted using antibody assays with imperfect specificity and sensitivity, and these characteristics exhibit substantial variation across assays. Moreover, the implications of these characteristics depend on the actual level of prevalence, e.g., adjusting for specificity is crucial in a context of relatively low prevalence.[23] Consequently, all three of the preceding meta-analyses consistently used seroprevalence estimates and confidence intervals that had been adjusted for test sensitivity and specificity using the Gladen-Rogan formula and/or Bayesian methods.[5, 8, 9] By contrast, this meta-analysis simply uses raw seropositive data from those studies that did not report test-adjusted seroprevalence.
Low Prevalence. The shortcomings of this manuscript’s approach are particularly evident in assessing IFRs for locations with relatively low prevalence. For example, as shown in manuscript Table 1, the seroprevalence study of Hungary used the Abbott Architect IgG assay to analyze 1454 specimens and obtained 9 positive results, i.e., raw seropositivity of 0·6%. According to the manufacturer’s data submitted to the U.S. Food and Drug Administration, this assay has sensitivity of 100% and specificity of 99·6%.[24] Consequently, the Gladen-Rogan formula indicates that the test-adjusted prevalence is only 0·2%, i.e., only one-third of the observed seropositive results were likely to be true positives. Moreover, this test-adjusted estimate has a 95% confidence interval of 0 to 0·4%, i.e., the prevalence is not statistically distinguishable from zero, and hence its IFR does not have a well-defined confidence interval. Indeed, that was precisely the reason why this cohort was not included in the meta-analysis of Levin et al. (2020).
Unmeasured Antibodies. This manuscript follows a completely unorthodox approach in adjusting seroprevalence for unmeasured antibodies: “When only one or two types of antibodies (among IgG, IgM, IgA) were used in the seroprevalence study, seroprevalence was corrected upwards (and inferred IFR downwards) by 10% for each non-measured antibody.” (p.8) This approach is particularly objectionable when applied to test-adjusted seroprevalence results, since those estimates have already been adjusted to reflect sensitivity and specificity. Moreover, such an approach has never been used by any other epidemiologist or statistician, in the context of the COVID-19 pandemic or for any other purpose, and hence should not be applied in a meta-analysis without providing any compelling rationale for doing so.
Seroreversion. The manucript “explores” the issue of seroreversion using proportionality factors based on the timing of each seroprevalence study relative to the preceding peak of COVID-19 deaths. However, the manuscript provides no rationale for following this approach instead of the rigorous Bayesian methodology utilized in a preceding meta-analysis.[9] Moreover, the manuscript makes no reference to the findings of longitudinal studies of the evolution of antibodies in confirmed positive individuals, which have concluded that the degree of seroreversion is substantial for some assays and negligible for others.[25, 26]
Measurement of Fatalities. Data on COVID-19 fatalities should be obtained directly from official government sources, not from media reports, web aggregators, or Wikipedia. For example, the European Center for Disease Control has an online COVID-19 database with daily data on reported cases and fatalities for nearly every country in the world. Moreover, whenever possible, fatalities should be measured using official tabulations of case data (based on actual date of death) rather than real-time reports that may be relatively incomplete and subject to substantial revision over time. These issues are particularly relevant for assessing fatalities in nursing homes: If a patient tested positive for COVID-19 and died soon thereafter, investigation would be needed to determine whether the death resulted from COVID-19 or unrelated causes. To illustrate these issues, consider the manuscript’s estimate of IFR based on the U.S. national seroprevalence study of Kalish et al. (2021). As shown in table 1 and appendix table 2 of this manuscript, the U.S. CDC case database (accessed in February 2021) indicates a total of 103862 deaths for adults ages 70+ as of 04 July 2020. To determine the corresponding fatalities in U.S. nursing homes, however, the manuscript relies on a news summary dated 26 June 2020 that reported a total of 52428 nursing home deaths in 41 U.S. states.[27] Using that real-time report, manuscript infers a somewhat higher national total of 57291 nursing home deaths and hence 46571 deaths outside of nursing homes. By contrast, the U.S. CMS case database (accessed in August 2021) indicates 38239 deaths in U.S. nursing homes as of 05 July 2020.[28] Evidently, there were 65623 fatalities outside of nursing homes, implying a correspondingly higher IFR of 3·6% for U.S. community-dwelling adults ages 70+.
Developing Countries. The use of confirmed COVID-19 fatalities can be highly misleading in assessing IFRs of developing countries, where testing capacity has been much more limited than in Europe or North America. Consequently, in developing country locations, the measure of fatalities should include both confirmed and suspected COVID-19 cases, or alternatively, a measure of excess deaths relative to preceding years. Indeed, several recent studies of India have concluded that confirmed COVID-19 fatalities understate the true death toll by an order of magnitude.[29-31]
Younger Age Groups. The manuscript states that “the studies considered here offered a <br /> prime opportunity to assess IFR also in younger age strata” (p.9) even though such analysis <br /> had not been proposed in the protocol. Nevertheless, this secondary analysis is at odds with the key eligibility criterion of this meta-analysis, namely, seroprevalence studies with at least 1000 participants ages 70+. Indeed, imposing that eligibility criterion leads to the exclusion of numerous other seroprevalence studies that would be highly informative for analyzing IFRs of younger adults, with an unknown degree of bias associated with that exclusion.
Self-Citations. A meta-analysis is intended to serve as an objective synthesis of information extracted from existing studies. Consequently, methodological decisions and substantive claims should not be based solely on citations of the authors’ own prior work. For example, in discussing the preceding meta-analysis of Levin et al. (2020), the manuscript asserts that “almost all included studies came from hard-hit locations, where IFR may be substantially higher”, with a sole citation to Ioannidis (2021a). However, that assertion is clearly false: The meta-analysis of Levin et al. (2020) included locations such as Australia, New Zealand, Ontario, and Salt Lake City that experienced very few infections during the first wave of the pandemic. Similarly, the manuscript asserts that “selection bias for studies with higher seroprevalence and/or higher death counts may explain why their estimates for middle-aged and elderly are substantially higher than ours” (p.14), with a sole citation to Ioannidis (2021b).
References Cited Here:<br /> 1. Ferguson N, Laydon D, Nedjati-Gilani G, et al. Report 9: Impact of non-pharmaceutical interventions (NPIs) to reduce COVID-19 mortality and healthcare demand2020.<br /> 2. Mizumoto K, Kagaya K, Zarebski A, Chowell G. Estimating the asymptomatic proportion of coronavirus disease 2019 (COVID-19) cases on board the Diamond Princess cruise ship, Yokohama, Japan, 2020. eurosurveillance. 2020;25(10). doi:10.2807/1560-7917.ES.2020.25.10.2000180<br /> 3. Salje H, Tran Kiem C, Lefrancq N, et al. Estimating the burden of SARS-CoV-2 in France. Science. 2020;369(6500):208-11. doi:10.1126/science.abc3517<br /> 4. Verity R, Okell LC, Dorigatti I, et al. Estimates of the severity of coronavirus disease 2019: a model-based analysis. lancet infectious diseases. 2020;20(6):669-77. doi:10.1016/S1473-3099(20)30243-7<br /> 5. Levin AT, Hanage WP, Owusu-Boaitey N, Cochran KB, Walsh SP, Meyerowitz-Katz G. Assessing the age specificity of infection fatality rates for COVID-19: systematic review, meta-analysis, and public policy implications. European Journal of Epidemiology. 2020;35(12):1123-38. doi:10.1007/s10654-020-00698-1<br /> 6. Williamson EJ, Walker AJ, Bhaskaran K, et al. Factors associated with COVID-19-related death using OpenSAFELY. Nature. 2020. doi:10.1038/s41586-020-2521-4<br /> 7. Mak JKL, Kuja-Halkola R, Wang Y, Hägg S, Jylhävä J. Frailty and comorbidity in predicting community COVID-19 mortality in the U.K. Biobank: The effect of sampling. Journal of the American Geriatrics Society. 2021;69(5):1128-39. doi:https://doi.org/10.1111/jgs...<br /> 8. O’Driscoll M, Ribeiro Dos Santos G, Wang L, et al. Age-specific mortality and immunity patterns of SARS-CoV-2. Nature. 2021;590(7844):140-5. doi:10.1038/s41586-020-2918-0<br /> 9. Brazeau N, Verity R, Jenks S, al. e. COVID-19 Infection Fatality Ratio: Estimates from Seroprevalence. 2020. doi:https://doi.org/10.25561/83545.<br /> 10. Arora RK, Joseph A, Van Wyk J, et al. SeroTracker: a global SARS-CoV-2 seroprevalence dashboard. The Lancet Infectious Diseases. 2020. doi:10.1016/s1473-3099(20)30631-9<br /> 11. Sullivan PS, Siegler AJ, Shioda K, et al. Severe Acute Respiratory Syndrome Coronavirus 2 Cumulative Incidence, United States, August 2020–December 2020. Clinical Infectious Diseases. 2021. doi:10.1093/cid/ciab626<br /> 12. Merkely B, Szabo AJ, Kosztin A, et al. Novel coronavirus epidemic in the Hungarian population, a cross-sectional nationwide survey to support the exit policy in Hungary. Geroscience. 2020;42(4):1063-74. doi:10.1007/s11357-020-00226-9<br /> 13. Perez-Saez J, Lauer SA, Kaiser L, et al. Serology-informed estimates of SARS-CoV-2 infection fatality risk in Geneva, Switzerland. The Lancet Infectious Diseases. doi:10.1016/S1473-3099(20)30584-3<br /> 14. Stringhini S, Wisniak A, Piumatti G, et al. Seroprevalence of anti-SARS-CoV-2 IgG antibodies in Geneva, Switzerland (SEROCoV-POP): a population-based study. The Lancet. 2020;396(10247):313-9. doi:10.1016/s0140-6736(20)31304-0<br /> 15. United Kingdom BioBank. UK Biobank SARS-CoV-2 Serology Study Weekly Report - 21 July 2020. 2020.<br /> 16. Ward H, Atchison CJ, Whitaker M, et al. Antibody prevalence for SARS-CoV-2 in England following first peak of the pandemic: REACT2 study in 100,000 adults. medRxiv. 2020:2020.08.12.20173690. doi:10.1101/2020.08.12.20173690<br /> 17. Hughes EC, Amat JAR, Haney J, et al. Severe Acute Respiratory Syndrome Coronavirus 2 Serosurveillance in a Patient Population Reveals Differences in Virus Exposure and Antibody-Mediated Immunity According to Host Demography and Healthcare Setting. The Journal of Infectious Diseases. 2020;223(6):971-80. doi:10.1093/infdis/jiaa788<br /> 18. U.K. Public Health England. Weekly Coronavirus Disease 2019 (COVID-19) Surveillance Report, Week 32. 2020. <br /> 19. Canadian Blood Services and COVID-19 Immunity Task Force. Final Results of Initial Canadian SARS-Cov-2 Seroprevalence Study Announced. 2020. <br /> 20. Dodd RY, Xu M, Stramer SL. Change in Donor Characteristics and Antibodies to SARS-CoV-2 in Donated Blood in the US, June-August 2020. JAMA. 2020;324(16):1677-9. doi:10.1001/jama.2020.18598<br /> 21. Bajema KL, Dahlgren FS, Lim TW, et al. Comparison of Estimated Severe Acute Respiratory Syndrome Coronavirus 2 Seroprevalence Through Commercial Laboratory Residual Sera Testing and a Community Survey. Clinical Infectious Diseases. 2020. doi:10.1093/cid/ciaa1804<br /> 22. Boyce RM, Shook-Sa BE, Aiello AE. A Tale of 2 Studies: Study Design and Our Understanding of Severe Acute Respiratory Syndrome Coronavirus 2 Seroprevalence. Clinical Infectious Diseases. 2020. doi:10.1093/cid/ciaa1868<br /> 23. Gelman A, Carpenter B. Bayesian analysis of tests with unknown specificity and sensitivity. Journal of the Royal Statistical Society: Series C (Applied Statistics). 2020;n/a(n/a). doi:10.1111/rssc.12435<br /> 24. U.S. Food and Drug Administration. EUA authorized serology test performance. 2020.<br /> 25. Dan JM, Mateus J, Kato Y, et al. Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection. Science. 2021;371(6529):eabf4063. doi:10.1126/science.abf4063<br /> 26. Muecksch F, Wise H, Batchelor B, et al. Longitudinal Serological Analysis and Neutralizing Antibody Levels in Coronavirus Disease 2019 Convalescent Patients. The Journal of Infectious Diseases. 2020;223(3):389-98. doi:10.1093/infdis/jiaa659<br /> 27. Kaiser Family Foundation. This Week in Coronavirus: June 18 to June 25. 2020. <br /> 28. U.S. Center for Medicare & Medicaid Services (CMS). COVID-19 Nursing Home Data. 2021. <br /> 29. Anand A, Sandefur J, Subramanian A. Three New Estimates of India’s All-Cause Excess Mortality during the COVID-19 Pandemic. Center for Global Development. 2021. <br /> 30. Deshmukh Y, Suraweera W, Tumbe C, et al. Excess mortality in India from June 2020 to June 2021 during the COVID pandemic: death registration, health facility deaths, and survey data. medRxiv. 2021:2021.07.20.21260872. doi:10.1101/2021.07.20.21260872<br /> 31. Shewade HD, Parameswaran GG, Mazumder A, Gupta M. Adjusting Reported COVID-19 Deaths for the Prevailing Routine Death Surveillance in India. Frontiers in Public Health. 2021;9(1045). doi:10.3389/fpubh.2021.641991
On 2021-10-12 14:55:07, user Ho Hum wrote:
The study was based on vaccination's done over a 2 month period. I could see that 32K might be too low but 800K seems too high considering that the entire population of Ottawa is just under 1 million. Did they vaccinate 80% of the population of Ottawa in just two months?
Something very wrong here.
The 1 in 1000 could be valid for the age 16-25 group. I could see a total of 32K of this demo being vaccinated in two months.
Too bad the researchers lost all their credibility over bad math
On 2021-10-12 23:46:26, user M Koltai wrote:
This preprint is now published at: https://wellcomeopenresearc...
On 2021-10-13 14:52:47, user Stephen B. Strum wrote:
Everyone has their unique response to an antigen, be it natural or a vaccine. The proof of the pudding is the end response relating to protection--from severe illness, to chronic COVID-19, to hospitalization, to needing an ICU, and to death. For certainty--being vaccinated is better than not. For breakthrough infections the data "appears" that Moderna is superior to Pfizer--but how about an analysis of those who had breakthrough infections? Age, Sex, BMI, Diabetes, Immune status, Medications, etc? I have not read the full paper but going through the publication I do not see that mentioned. How about a probably surrogate or correlate of protection in the form of total immunoglobulin (Ig) G against the S1 protein as measured by the LabCorp or Quest Roche Elecsys test? In my case (age 79, light chain amyloidosis in complete remission (CR) & off chemo or immunotherapy x 1 year) my SARS-CoV-2 Ab (antibody) level at 1 month post two doses of Pfizer was > 250 U/ml, only to drop to 59 at 4 months. Then, I received a Moderna booster on 9/1/21 & on 10/5/21 my Ab level was > 2,500 U/ml. These are tests that are commercially available. The results are back in 24 hrs; the test is not expensive. There's a huge difference in individuals, especially by age and by comorbidity. <br /> LabCorp test code 164090: SARS-CoV-2 Semi-Quantitative Total Antibody, Spike using Roche Elecsys. <br /> Quest Test Code 39820 SARS-CoV-2 Total Antibody, spike, semi-quantitative using Roche Elecsys. <br /> With the huge # of publications on COVID-19, there should be articles correlating the level of IgG vs. breakthrough infections. Where is that article(s)??<br /> Stephen B. Strum, MD, FACP
On 2021-10-15 22:17:00, user baruch1014 wrote:
so the gist of what i read here is that people who developed encephalopathy due to the severity of infection were more at risk for neurologic and psychiatric issues six months post-infection... but, i mean, you could contextually make the same determination with regard to auto accident survivors who develop encephalopathy in relation to the severity of the auto accident, or mma fighters, or football players, or people who have almost drowned or otherwise were deprived of oxygen to the brain... am i incorrect? basically, any trauma to the brain, if severe enough, can cause later psychiatric or neurologic affects.
On 2021-10-16 11:50:49, user Markus Falk wrote:
Very interesting read. Does the unvaccinated group contain persons with a past infection?
On 2021-10-25 17:08:33, user Arron190 wrote:
It would be interesting to see how the data changes if those with naturally acquired immunity (ie been infected) are removed.<br /> Around 13% of US citizens have been infected so far.<br /> Many of the uninfected may be interested to know what level of protection the vaccine provides.
On 2021-10-16 23:35:24, user Mike New wrote:
Here is the pertinent question that I would like a straight answer on:
Does the Singapore study suggest that a vaccinated person is more likely to be "asymptomatic" with the delta strain than an unvaccinated person ? yes or no ?
On 2021-10-18 00:04:56, user Geoffrey Graham wrote:
An encouraging study! Mobile HEPA filters may do a great deal of good.
Cigarette filters can also remove aerosols of biologically relevant sizes from an air stream. Seventy-five half-length filters in parallel will transmit enough air for a facemask wearer to breathe comfortably. Cigarette filters are very common around the world and so are other materials from which facemasks could be made. Building a 75-filter facemask from these materials is straightforward. If cigarette filters can also remove SARS-CoV-2 from an air stream (this needs to be tested), we could save a lot of lives this winter.
Here is a brief account of where things stand:<br /> See “The Saga of the Universal Anti-COVID Facemask: Where Things Stand”<br /> at:<br /> https://geoffreyjgraham.sub...
And here is a comprehensive (read “gargantuan”) account of all significant results.<br /> http://distributiveeconomic...
Clearly, the cigarette filters must be tested against actual virus. I am soliciting advice on the best way to do this. Beyond this, I welcome advice on what to do (and what not to do) next.
Geoff Graham<br /> gjgraham4health@protonmail.com
On 2021-10-18 14:09:02, user S Wood wrote:
peer reviewed version now at
On 2021-10-19 16:26:22, user Andy Bloch wrote:
There was a significant (and substantial) statistical difference that they brushed off, and they included the first 2 weeks after injection in the comparison. Pfizer is clearly more effective than AZ after 2 weeks against positive tests, as the Hazard Ratio chart in their Figure 2 shows.<br /> https://twitter.com/Andy_Bloch/status/1450397100341035021
On 2021-10-20 03:04:28, user Noriaki Kurita (????), MD, PhD wrote:
This preprint has been published by BMC Health Services Research. <br /> https://bmchealthservres.bi...
On 2021-10-21 13:28:45, user CDSL JHSPH wrote:
Dear Authors,
This Study was extremely consequential and extremely well constructed. Particularly in the advancements in identifying previously unknown areas responsible for atrial flutters via utilization of electroanatmocal mapping systems. The triad of identification from density based maps, definition of criteria in voltage density and tachycardic cycle length are great strategies in looking at these complex cases. A few critiques I would however like to levy though is that due to the large amounts of technical jargon within this paper especially displayed within the raw data output by the EAM systems. Further explanation of the data in the figures and results would improve the overall readability of the study and contextualize further on the crucial outcomes. Another point I believe already brought up is due to the low number of patients in the cohort and the survivorship bias in all cases, the true possibilities of the CARTO EAM based mapping systems have yet to be evaluated. The last critique I would like to present is I was extremely curious regarding the radiofrequency doses administered between numbers of VALLEYS when treated I would assume longer times of treatment as well as larger dosages as more areas were responsible for these arrhythmias and would greatly clarify some of the data presented in the second Table. However this paper was extremely enjoyable to sift through and thank you for your work!
On 2021-10-24 02:36:03, user randy tangang wrote:
The great work in the analysis of how gut microbiome BA dysregulation can increase the risk of immune or metabolic disorders. As it was pointed out in the paper, lifestyle was one of the factors that were left out in this analysis of gut microbes. One factor that I thought was very important was how the environment had an influence on these microbes. The experiment used just 3 countries and all in one continent and as I know, people in different continents are exposed to different bacteria and turn to harbor different bacteria in their guts depending on the environment they live in. someone in the western world (Europe) who has access to clean water and different antibiotics in their food will have a different gut microbiome BA from someone who lives in Africa or South America where people are exposed to many bacteria on daily basis. The paper talks about using this analysis for therapeutic targets in immune or metabolic disorders. And so if the end goal is to use this universally, I recommend studying and analyzing how different environments affect gut microbes BA in different continents.
On 2021-10-25 21:40:02, user John Hulleman wrote:
This preprint was subsequently published in Molecular Vision on April 2nd, 2021. Please see link below for the accepted article:
On 2021-10-26 09:42:04, user Stephen Hinkle wrote:
I think this study calls for an important discussion about how we approach COVID-19 in the future. I think that it is clear that people can get this more than once. Other studies have shown that vaccine immunity is not lifelong either. I think we need to INFORM THE GENERAL PUBLIC OF THIS TRUTH and have a public policy discussion where the public is invited to participate on how the public wants to confront COVID-19 longer term going forward. It is likely that this will be an endemic virus (this is the conclusion of many top public health universities including Brown, Harvard, Stanford, Johns Hopkins, University of Minnesota, Imperial College London, University of Alabama at Birmingham, University of Arizona, University of Sydney, University of Queensland, Oxford, and others). Many countries have abandoned their "Zero Covid" strategies as well realizing this including Australia, New Zealand, Vietnam, Thailand, Singapore, and others. This study covering Iran shows that people got infected many times.
Do we stay in lock down and abandon some activities and pleasures in life forever possibly leaving businesses permanently closed or forcing everyone to say their last goodbye to our friends, abandon all group activities, sports, performing arts, dating, and our pleasures in life forever in an attempt to stay alive or stop the virus? Do we open up and accept the risk of ongoing community spread of COVID-19 and keep getting booster shots for individual immunity and new variants? Should getting vaccines be mandatory or an individual level decision? How do we protect the immunocompromised and those who are more vulnerable or who the vaccines do not work well on? Do we do a massive COVID-19 testing operation and try to eliminate the virus through daily tests and quarantine people if they are infected an allow the others to go on with normal life activities? What level of death and disability should society choose to accept to have the levels of freedom of movement and/or non-household member social interaction we want in the future if the COVID-19 virus will be endemic? Should shuttered sectors of the economy be allowed to reopen or not? Should in-person schooling continue or not? Should masks be required indefinitely or should it be optional or not required?
I think it is time to start a policy conversation with the GENERAL PUBLIC to determine what they want the un-perfect pandemic endgame to be in terms of living with the virus and going on with life as safe as we can but it is likely the day-to-day risk will not be zero. It is clear to me based on all the recent evidence from this study and all the current data trending in other recent studies is showing that COVID-19 will become ENDEMIC and that this pandemic is going to have a social ending as opposed to a eradication or herd immunity outcome most likely. But the real question now is what will a divided public tolerate in terms of COVID-19 policy longer term and what is the public health end goal now? Maybe it is time to ASK THE GENERAL PUBLIC FOR IDEAS here.
Personally, I think that the COVID-19 pandemic is another case of humans showing a poor record of eradicating diseases.
On 2021-10-26 17:04:29, user Robert wrote:
In the history of Vaccines I have yet to see where a drug company is not working on a new or altered vaccine within 6 months of the original. Given the speed these vaccines were released you would think that alternate or new and improved mRNA would be released or spoken of. I have seen nothing or read nothing. <br /> Additionally. This is the only vaccine I ever seen pushed that does not have the listed side affects.
On 2021-10-26 21:25:43, user Eugene Peskin wrote:
The article doesn't provide much clarity how the number of cases among the non-immune was actually calculated.<br /> If accomodation for immune layer of 46% has been done to re-calculate attack rate for control group, it should also be accomodated for the main group calculation, as 46% one-time vaccinated already had immunity before vaccination (actually less, you should deduct those who got their immunity from previous vaccination).
On 2021-11-07 15:28:01, user DinCville wrote:
What can a study of 60+ year olds who had breakthrough infections tell us about the risk for all 60+ who are vaccinated? How representative are those 60+ with breakthrough infections? Could they be more likely to have pre-existing conditions that affected the effectiveness of their vax response? Concerned that these results be interpreted to mean all 60+ with vax are unprotected from long covid.
On 2020-04-22 20:38:01, user David Swiff wrote:
Macrolides can prolong the QT and QTc interval and cause cardiac arrhythmias, including TdP, ventricular tachycardia, and ventricular fibrillation, via their effect on the IKr potassium channel.
On 2020-04-23 05:17:25, user B Yabut wrote:
The authors forgot the known main mechanism by which hydroxychloroquine works. Late administration at the point needing intubation means the cytokine storm has alreadybeen set in motion. Biomolecular and cellular studies showed that hydroxychloroquine works at the point of viral cellular entry and early inside the cell. Granted it also has a still unelaborated effect on the inflammatory process the study from France specifically included the pre-condition "Early administration."
On 2020-04-24 00:57:17, user Philip Davies wrote:
Well, well well ...
This pre-print would make a good script for an episode of Columbo.
The retrospective analysis, as presented, leads the reader to just one conclusion in a bazaar of many possible conclusions.
I am even starting to have sympathy with D. Raoult and his team. I note his hot tempered response to this paper, where he lists two enormous factors that should be considered when wrestling with the data: the fact that the HCQ and HCQ & AZ cohorts were a sicker crowd (he lists lymphopenia) and that the sickest of the non-HCQ ventilated patients were then given HCQ (plus AZ in most cases) in a desperate last bid only for most to die.
Raoult's point is certainly valid.
We must remember that for most of the study period the use of HCQ was "ex-license" on a compassionate basis only. This means only the sickest patients got it. Remember also that this is a retrospective analysis, therefore observational. It was not run as a therapeutic trial. On the other hand, the use of AZ was already accepted (hence 30% of the non-HCQ cohort got it anyway).... although do be aware that by this time there had been quite a lot of focus on potentially dangerous QT lengthening when HCQ and AZ were used together in very sick patients.
The HCQ cohort was, across all key determinants, the weakest and sickest group (it had the poorest prospects looking at age, ethnicity, smoking status, congestive heart failure, peripheral vascular disease, cerebrovascular disease (strokes),dementia, COPD, Diabetes (with and without complications)! ... and indeed, the HCQ and HCQ & AZ cohorts did have 100% more lymphopenia than the non-HCQ group.
BUT, the big asymmetric issues become obvious when we look at the pre- and post- ventilator numbers.
In terms of patients discharged without needing ventilation, the "victorious" non-HCQ group performs poorer than the 2 treated groups. This despite having a better prognostic baseline. But the results for this group change dramatically (for the better) when we look at the outcomes of ventilation. 25 ventilated patients came from this group.... but 19 of these 25 patients were then started on HCQ or HCQ & AZ after ventilation was started. It is screamingly obvious that these would be the sickest patients in that group: they were given such compassionate drugs in extremis. So having ejected 19 of 25 ventilated patients into the other cohorts, the non-HCQ group only had 3 deaths from its remaining 6 ventilated patients.
The numbers of ventilated patients in the other cohorts (HCQ and HCQ & AZ) were thus substantially inflated with these new super-sick patients, who mostly died.
There really can be no conclusion at all when looking at a study of this nature without knowing much more about individual clinical conditions and guiding principles behind clinician's decision making. It's still possible to make some reasonable assumptions:
If I were Columbo?... I would say the non-HCQ cohort contained patients of extremes, with the best and worst potential. The worst would have been the very frail (malignancy and or congestive heart failure maybe ... see the stats), who probably were earmarked for 'supplemental oxygen' only from the very start. Such patients would not have been suitable for compassionate use of non proven drugs (remember, most of this came before the "emergency use" edict by FDA). This would explain the number of non-ventilated patients who died in this group (they may have been given AZ only, not being a controversial drug, but otherwise they did not get any significant interventional therapy). These patients would have had significant chronic disease and very poor obs/indices (including lymphopenia). But given that this cohort had, overall, a better starting prognosis than the other two groups, it means that the remaining patients in the group were promising candidates for survival (with better obs/indices). Such patients, not being part of a clinical trial, would not have been offered HCQ on a compassionate basis unless they got dramatically worse .... and of course, the ones who did get worse on the ventilator were started on HCQ (& often AZ as well) and thus swapped into the HCQ / HCQ & AZ cohorts.
If we can understand that, then we might start to think that in fact HCQ & AZ is the best performing cohort with the other 2 vaguely distant. But this is being unfair to the HCQ cohort:
The reason that a sick patient would be given one experimental drug on a compassionate basis (HCQ) but not have a rather less experimental drug further added (AZ), can really only be explained by considering risk versus benefit. A clinician would choose to use HCQ because the patient was particularly sick. The clinician would only add AZ if it was felt that this was worth the risk.... but a particularly sick patient with significant cardiovascular disease (the HCQ contained the most CVD risk) might then die of a more abrupt arrhythmia through adding yet another QT lengthening drug. I dare say the clinicians were tempted to make some "Hail Mary" plays, but we must remember, these patients were not part of an ongoing trial, these drugs were "ex-license" for compassionate use only and clinicians were still accountable for responsible actions. So for those particularly sick frail patients, it wasn't worth the risk.
I am pretty sure that the HCQ cohort (which had pretty good pre-ventilator stats) crashed badly because it was loaded with the sickest patients .... patients that were too sick to risk adding AZ.
So, the findings of this retrospective analysis are, in my opinion, likely to be incorrect.
I believe I can confidently state that:
It is almost impossible to reach a conclusion from all this. BUT, the most likely finding is NOT that adding HCQ delivers a worse outcome than standard treatment. In fact, if we look at the pre-ventilator stats, the addition of HCQ might actually have provided considerable benefit to a particularly sick group of patients. Whether or not the addition of AZ to HCQ adds benefit is also unclear ... although my 'swingometer' is pointing slightly more to benefit than harm.
Once again. I suggest that a robust study into prophylaxis and early treatment (using sensible safer doses adjusted for pulmonary sequestration) will deliver the most interesting results for CQ/HCQ.
Dr Phil Davies<br /> Aldershot Centre For Health<br /> http://thevirus.uk
On 2020-04-24 04:44:30, user joe2.5 wrote:
I don't know if I'm the only one to totally miss, in this paper, the main point I should be paying attention to. Anecdotal data that started the idea that OH-chloroquine could be of value in treating Covid-19 indicated quick decrease of the viral load hen administered just at the start of symptoms or even before. I read the paper twice without being able to see any mention of the time from first symptoms to treatment. So the impression is that the study was not trying to answer the initial question.
On 2020-04-23 00:19:12, user Michael S. Y. Lee (biologist) wrote:
Hello,
Did you infect Vero-E6 cells from each patient just once (and harvest the cells in quadruplicates), or did you infect the Vero-E6 cells from each patient four times (and harvest the cells once per infection).
This is very important for statistics.
Mike
On 2020-04-24 14:35:40, user VirusWar wrote:
Interesting study. some comments :<br /> 1. The increase of QTc can be due as well to renal diseases due to COVID19, Such renal diseases were pointed in this study "The QT Interval in Patients with SARS-CoV-2 Infection Treated with Hydroxychloroquine/Azithromycin" https://www.medrxiv.org/con...<br /> Renal diseases cause big levels of Potassium in the blood and increase QTc, so the level of Potassium should be checked as well, especially when QTc>=460 ms. If level of Potassium is high, action can taken (like treat renal disease, eat less Potassium, extra magnesium given). In some cases (QTc >460 ms and QTc<500ms), risk seems manageable. <br /> 2. There is no point to use hydroxychloroquine for severe patients. It takes 3 days to have effect on early stage, in combination with azithromycine. For severe patients, there are usually not much virus left but big damages, so it is too late to give hydroxychloroquine.
On 2020-04-24 14:59:19, user Tomas Hull wrote:
"New York antibody study estimates 13.9% of residents have had the coronavirus" Gov. Cuomo says<br /> https://www.cnbc.com/2020/0...
Congrats, Dr. Witkowski. You stand vindicated...
On 2020-04-25 01:25:07, user Brent Tharp wrote:
Not even close to the real numbers, which are 50 to 100 times greater.
On 2020-06-08 19:23:59, user Animesh Ray wrote:
This is an interesting study, but the conclusions should be considered with caution. The causal modeling used here "suggest" that the chosen data are consistent with the hypothesis that Vitamin D deficiency might be correlated with increased morbidity of COVID-19. There are several caveats, however. (1) In meta-analysis of this sort, it is very difficult to be quantitative unless the observed data of the same data-type are shown to be at least comparable in variance. I did not see an effort to establish that. (2) Even though statistical analysis by multiple regression is precluded because the data were obtained from different sources, at least an effort to center the various data around means and doing a multiple regression to ascertain the magnitude of the variables' effects and their interactions would have been interesting. The problem here is that there are so many explicit variables and so many hidden ones in each experimental datasets, it is rather difficult to pinpoint any one--in this case vitamin D status--as causal. As von Neumann once stated, 'Give me four variables and I will make an elephant out of them; give me five, I will make it wave its trunk'. (3) Finally, the authors' molecular explanation--that Vitamin D inhibits rennin-angiotensin axis--is as easily explained in favor of the model as against the model (e.g., a lowered expression of ACE2 receptor due to inhibition by vitamin D might enable SARS-CoV-2 viruses to saturate these receptors far more easily than if the receptors are normally expressed, thus precipitate the loss of blood pressure control and cardiac output more readily than otherwise. In other words, the effect of normal vitamin D could enhance, not prevent, SARS-CoV-2 virus's clinical impact.) Thus the value of the molecular causality, as claimed by the authors, as a critically falsifiable test is doubtful. Nonetheless, many epidemiological success stories are built upon causal inferences based on precisely this type of analysis: one can cite examples of cholera on shallow wells in London in 18th century, scurvy and vitamin C, and now well established role of vitamin A and general resistance to childhood infections. On that basis, the idea that vitamin D might indeed be protective against COVID-19 complications merits further study.
On 2020-04-25 15:20:13, user Alex Backer wrote:
Very nice analysis. Here is a paper from 3 weeks ago that is very relevant to this: https://ssrn.com/abstract=3... (The Impact of Solar Irradiance on COVID-19). <br /> These two are relevant as well:<br /> https://ssrn.com/abstract=3... (Why African Americans are dying more)<br /> https://ssrn.com/abstract=3... (Why Latinos are dying less)
On 2020-04-25 18:13:47, user Pavel Valerjevich Voronov wrote:
What I do afraid - delays with vaccine because not taking that study in to account. Imagine, if they inject vaccine to mostly O- subjects, having promising results, move forward, then it "accidentally" won't work with others. Vaccines must be evaluated with A+ recipients at first, I suspect. Or at least blood type should be taken in consideration while results evaluation - A+ MUST be present. Even if this study is not finished - such testing approach shouldn't be harmful.
On 2025-02-26 18:14:55, user Benjamin Isaac wrote:
Reference 12, referring to the article here https://pmc.ncbi.nlm.nih.gov/articles/PMC8784688/ doesn't list the journal or date. The APA citation would be: Patterson, B. K., Francisco, E. B., Yogendra, R., Long, E., Pise, A., Rodrigues, H., Hall, E., Herrera, M., Parikh, P., Guevara-Coto, J., Triche, T. J., Scott, P., Hekmati, S., Maglinte, D., Chang, X., Mora-Rodríguez, R. A., & Mora, J. (2022). Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) up to 15 Months Post-Infection. Frontiers in immunology, 12, 746021. https://doi.org/10.3389/fimmu.2021.746021
On 2020-05-04 18:24:02, user Dan Kammen wrote:
The full data sets and code can also be accessed here:
On 2025-09-02 10:12:20, user Audouze wrote:
Now published in Toxicology ( https://doi.org/10.1016/j.tox.2025.154225) "https://doi.org/10.1016/j.tox.2025.154225)")
On 2025-09-24 08:57:19, user Sophie PILLERON wrote:
This paper states that it uses the Globocan dataset; however, Globocan does not provide cancer incidence trends data. I suspect that the authors actually used CI5 data instead, which are available up to 2017.
In addition, this paper is very similar to another one ( https://pubmed.ncbi.nlm.nih.gov/34866023/ <br /> ), which the authors did not cite. The main differences between the two are the age groups analysed and the fact that the cited paper used data only up to 2012.
I would also recommend specifying the data source in the abstract, as this information is useful for interpreting the findings.
A justification for grouping all individuals aged 50+ together is needed, as this is a very heterogeneous age group. While I understand that the main focus of the paper is on the younger age group, the comparison would be more meaningful if the age categories used were more relevant.
I also suggest authors to reconsider the use of statistical testing. The study aim being descriptive, the use of statistical test is not needed as no a priori hypothesis are tested.
On 2025-09-25 01:05:32, user Florian Hladik wrote:
The abstract states, "we treated eight recipients with material from a single donor". However, it seems you treated four recipients with VMT and the other four with the placebo. Correct? It's confusing as written. In the Results too. Otherwise, great work! The other paper reporting the L. crispatus RCT is cool as well!
On 2025-09-30 03:53:09, user Eero Raittio wrote:
Published in Community Dentistry and Oral Epidemiology <br /> https://onlinelibrary.wiley.com/doi/10.1111/cdoe.70026
On 2025-10-14 23:19:52, user T. De La Cruz wrote:
On behalf of the authors, we would like to update to the medRxiv community that the present preprint is now published in a journal and available at https://doi.org/10.1016/j.ijidoh.2025.100078 .