274 Matching Annotations
  1. Oct 2017
    1. administration of either antibiotics or probiotics to, respectively, increase or decrease microbial numbers and diversity

      This sentence reads that antibiotics increase microbial diversity and probiotics decrease diversity. Is that what you mean?

  2. Jul 2017
    1. Our Gut Microbes Strongly Influence Our Emotional Behaviors

      Bacteriodes versus Prevatella = more rational versus more emotional. interesting.

  3. Jun 2017
    1. cell surface

      maybe start with which cells before you talk about molecules.

    2. symptomatically

      I don't think you mean to say it like this

    3. luctuating climates

      what does this mean? be specific

    4. recently

      give a date or change this to say "recent outbreak"

    5. transmission

      I don't think you mean "transmission" here

    6. The initial symptoms o

      rather than start with symptoms (organismal), talk about distribution prevalence, etc first.

    7. Enterovirus genus

      put references at the end of your sentences

    8. categorized alongside poliovirus

      say "is similar to"

    1. ers into the cell's cytosol.

      please refer to the figures so your reader knows when to look

    2. RME

      since you never use this again, there is no reason to make an acronym

    1. Caroline Beuligmann


    2. The viral envelope of the Marburg virus includes glycoproteins (GP) that acts as a ligand and interact, by binding or sending signals, with cellular molecules on the host cell surface (Takada).

      put the image reference here or better yet...stick the image here.

    3. Current findings suggest that almost anyone is a susceptible host for Marburg virus (Martines).

      start with this statement since you really want to emphasize that anyone can get it.

    4. a (See Figure 1 and Table 2)

      I suggest you set this up better so that the TWO images you insert to talk about outbreaks is given more weight in your text.

    1. released via budding.

      maybe bring back to the virus is now ready to infect a new cell

    2. hree proteins—P, V, and C.

      refer to figure here...makes your life so much easier

    3. Life cycle of the measles virus

      maybe put this as the first image since it is an overview.

    1. lipid rafts

      I don't think many people know what these are. you may want to include this concept in the figure 2

    2. peplomers

      I have never heard this before...how different from proteins?

    3. see figure 1

      This figure is at the molecular level...can you get a picture of the virus?

  4. May 2017
    1. Structure

      you need to write this down and put in a figure caption

    2. d negative-sense, single-strand RNA virus. This means that the virus has genetic material that consists of a single strand of RNA that has the opposite sequence to messenger RNA. Therefore, the genetic information must be converted by RNA polymerase in order to be translated into a protein and carry out its function. There are two major glycoproteins on the surface of RSV and they are called the attachment glycoprotein (G) and the fusion glycoprotein (F) (3). These proteins with sugar attached to them can be found in or around the membrane of cells, and ultimately play an important role in the initial phases of the infection (3).

      you may want to move this to the viral life cycle part

    1. Mastomys natalensis

      you could just say mouse....you made me look it up

    2. e Lassa virus

      refer to your figures in the text. Tell me when you want me to look at your figures. Also, give every figure a figure caption.

    3. Mild symptoms include slight fever, general discomfort or illness, weakness and headache. However, the other 20% of infected individuals experience more serious symptoms such as hemorrhaging in gums, eyes or nose, respiratory issues, nausea and vomiting, swelling in the face, pain in check back or abdomen and even shock. There have also been incidences of neurological problems including hearing loss, tremors, and brain swelling. In these cases, death may occur within two weeks of the first showing symptoms due to multi-organ failure [3

      put some numbers on these and move up before timeline

    4. animal borne

      which animals?

    5. the first to die from the disease.

      maybe describe the disease here.

    1. Vs) detected worldwide, July 2009 - March 2011 (29)

      refer to your figures in your text. tell me when you want me to look at them.

    2. There have been no serious side effects caused by IPV which is why there has been a pushed to change to vaccine method in order to reduce VDPV and eventually eradicate the disease.

      then why haven't we used it before?

    3. y Sabin wild type strains. Most commonly by wild type 3 and 2.

      not sure how these are related. maybe set this up a bit more

    4. at can grow in the gut of

      the vaccine virus can always replicate...that's the point

    5. attenuated

      what does this mean to you?

    6. positive stain of Poliovirus

      refer to your figure in your text. tell me when to look at it.

    7. reduced the polio cases.

      by 99% apparently

    8. pe 1 and 3 are currently foun

      what are the differences other than geographic distribution? maybe not bring this up here but integrate it into more specific details about the virus.

    9. paralysis.

      maybe start with the disease...

    1. quire their envelope

      you may want to draw this out.

    2. psids bud into the ER lumen.

      a little more detail here. I suggest that you talk about the genome (made where) is assembled in the cytoplasm. Then, the whole she-bang fuses into the ER (what?!) to pick up spike proteins.

    3. These polyproteins are cleaved by viral proteases to form a smaller proteins that form the viral replicase and allow the virus to synthesize a negative sense template and subgenomic postive sense RNAs. The negative sense template is used to produce the positive sense viral genome that will be encorporated in to new viruses, while the subgenomic RNAs encode all viral proteins.

      you can save this detail for the replication part. Here, you may want to focus on 1) making proteins needed for replication, 2) making more genome, 3) making structural proteins

    4. While research into the

      don't leave me hanging!

    5. tory drugs are the only treatment, since no

      three really big thoughts in a single sentence. break it up

    6. re severe respiratory problems


    7. There are also rarer symptoms including gastrointestinal symptoms such as diarrhea, which is important considering other coronaviruses cause gastrointestinal diseases

      how much rarer? worth mentioning?

    8. The disease is caused by new virus of the family coronaviruses (Groneberg, 2005). Viruses of this family are spherical, have an envelope, contain RNA which can be directly translated inside the host (positive sense RNA). Their surface is also covered in "spikes" of glyoproteins, which produce the "corona" effect under an electron microscope which gives them their name (Groneberg, 2005). The SARS coronavirus (SARS-CoV) genome was sequenced in 2003 and was distinct from any other coronavirus found in humans or human-associated animals (Groneberg, 2005).

      You are switching from outbreak (population) to molecular and back again. Try to keep all the same scales together.

    9. viral respiratory disease

      maybe talk a bit about the disease

    1. Congenital infection, however has much worse prognosis and a higher mortality rate (approximately 35%).


    2. Symptoms of LCM tend to present itself within 8 to 13 days after contracting the virus. There are various phases in which the infection presents itself as disease. The initial phase of the disease includes symptoms such as fever, malaise, lack of appetite, muscle aches, headache, nausea, and vomiting. After recovery from the initial phase, a second phase of illness may occur. Symptoms that coincide with the second phase of illness include meningitis (inflammation of the meninges), encephalitis (drowsiness, confusion, sensory disturbances), and meningoencephalitis (inflammation of the brain and the meninges).

      gives some numbers and context to the disease

    3. help them fight off infection

      usually that means that those people have been exposed prior.

    4. The Lymphocytic Choriomeningitis Virus (LCMV)

      why don't you start with disease and work your way to where the virus lives?

    1. The spread of smallpox has decreased dramatically.

      from devastating to eradicated is pretty dramatic. :-)

      You are mixing all of your ideas and facts here. i think you can reorganize based on population, organism, cell, molecular a bit better.

    2. A biopsy or x-ray can be performed to examine whether the patient is showing signs of a viral infection.

      biopsy of what? x-ray of what? is there a pneumonia? what are you trying to say?

    3. f symptoms that are general enough

      such as...?

    4. creates a localized pus-filled rash.

      in the respiratory tract? I don't think that is what you meant to say.

    5. making it highly contagious.

      lots of things are spread through respiratory droplets that are not as contagious. Your interjection about breathing is confusing here.

    6. s variola.


    7. of smallpox i

      why don't you talk about what the disease is?

    8. careful treatment of current patients with the disease, they made it possible.

      not sure what you mean here.

    9. family and functions as effectively as cowpox.

      it is cowpox. it is not easier to grow it does not cause gross deadly disease. It causes mild disease. The current vaccine is even more tame than the original.

    10. vaccinia

      what is this? you haven't talked about it yet.

    11. vaccinated. T

      Is this a story? flesh it out or take it out

    12. effective process for smallpox was confirmed,

      do you mean effective vaccination process?

    13. ollowing with smallpox r

      he didn't give them small pox after as part of the vaccine. He challenged them with small pox and they didn't get disease.

    14. o get vaccinated out of fear.

      don't call it vaccinated until you get to the Vaccinia strain.

    15. Edward Jenner played a key role in developing a vaccine for smallpox. Prior to his research, dried pus-filled scab material would be scratched onto a person's skin to expose the uninfected person to the disease.

      Put some timelines on this. you have 1980 and the next thing you say is Jenner...makes it sound like he was important in 1980. I'm pretty sure he was long dead before that time. Scarification was practiced at least 100 years before Jenner

    16. vaccination for smallpox decreased significantly in the early 1980s.

      how is vaccination rates declining important here. If eradicated, there is no need for a vaccine.

    17. h high mortality and contagious levels, fi

      put numbers on this..

    18. incredibly

      just devastating is fine.

    1. onomic and sanitary conditions

      if 98% of the population is exposed, it's pretty hard to make this claim. I think you mean people who show frank disease.

    2. r

      which is when?

    3. Some common symptoms of EBV include: fatigue, inflammation of the throat and lymph nodes, fever, rash, swollen liver, and enlarged spleen (2).

      start with this and lead with the "kissing disease"

    4. As stated earlier, humans are the primary reservoir for EBV. Though there is a great deal that is not clearly understood about the entry mechanisms used by EBV, there have been experiments done in vitro that provide the most probable mechanisms (1). In order for a successful entry into a B cell, an interaction between EBV glycoprotein called gp350 and a protein complement receptor called CR2/CD21 is needed (1). Once the virus binds to this respective site, it is endocytosed into a low pH compartment (1). This low pH environment helps initiate the fusion of the "core fusion machinery", which is a common mechanism of virus-cell fusion among all herpesviruses (4). This core fusion machinery contains four glycoproteins that help mediate fusion B-cell fusion (4). It is hopeful that future research will reveal these entry mechanisms of the EBV virus so a vaccine can be developed to provide immunity.

      save for the life cycle stuff

    5. virus is approximately 122-180 nm in diameter and is a double-stranded helix of DNA which contains about 172,000 base pairs and 85 genes (5). The DNA is surrounded by a protein shell called a nucleocapsid which is surrounded by clusters of protein called a tegument (5). This tegument then is surrounded by an envelope of lipids and surface projections of glycoproteins that are integral in the infection of the host cell (5).

      save for later. you want to stay at the same length scale (organism or population)

    6. s usually accompanied by a recovery period of two to four weeks i

      you are talking about recovery before you ever talk about disease. not everyone knows what mono is symptomologically.

    7. EBV causes infectious mononucleosis (mono) a

      start with this

    1. viral

      you might mean viable here

    2. HPIV can be efficiently removed from surfaces with most common detergents, disinfectants, or antiseptic agents.1

      you haven't told me how it is transmitted. so telling me how to get rid of it on surfaces seems premature

    3. zoonotic

      why add this vocab word if it doesn't apply?

    4. s children and the elderly.2 Other groups likely to show symptoms are those suffering from malnutrition, vitamin A deficiency, babies not being breastfed, and those exposed to environmental toxins such as smoke

      make into one sentence

    5. -2 is less detecte

      numbers. and maybe just say there are four forms that cause different types of disease and give numbers. You can dive into the weeds later.

    6. causing lower respiratory diseases.

      what does this mean? pneumonia? how is it related to flu? Start with stuff your reader will care about.

    1. 36% of all reported cases r

      does not jive with 50% above

    2. . Other rare cases a human can contract the virus is if an infected mice bites someone, or touch or eat anything that came into contact with infected mice droppings, urine, or saliva (CDC).

      you went from describing an outbreak (interesting!) and moved to transmission. tell your story one step at a time

    3. lation of aerosolized mouse droppings.


    4. ot spread from person to person.


    5. o several Native American Tribes.

      please explain how this bit of information is important to your story (it feels very "thrown in").

    6. four corners

      Capitalize "Four Corners"

    7. Hantavirus Cardiopulmonary Syndrome (HCPS), is mostly common in the western states. 96% of reported cases of HCPS have occurred in states west of the Mississippi River.

      meld these ideas with above

    8. ude fever, headache, muscle aches, and chills, and progresses to a severe respiratory disease that can eventually lead to death

      numbers? denominator?

    9. the deer mouse was the primary carrier of the virus

      stay with one thought at a time. stay with disease, outbreak.

    10. re was an outbreak in the southw

      give numbers and more details...

    11. rdiopulmonary Syndrome in humans

      in text citations and what does this look like?

    1. Human adenoviruses lack a viral envelope composed of proteins and lipids that surround the viral capsid (1). They are generally 65nm to 80nm in diameter, and are composed of a protein capsid and a nucleoprotein core that contains the viral genome (double-stranded DNA, 26-46 kbp, containing 23-46 protein coding genes) (1). Depending on the viral subgroup, the human adenovirus has a range of diversity (1). Within subgroups (A, B type 1, B type 2, C, D, E, F, G), the human adenovirus serotypes share between 48% and 99% of their DNA; between subgroups, however, there is less than 20% shared (1).

      save for later...too much molecular. think global, population, organism, cellular, then molecular

    2. AdV antibodies in their bodies, i

      what does this mean and why is it important?

    3. Human adenoviruses cause a number of diseases, most often conjunctivitis, gastroenteritis, hepatitis, myocarditis, and pneumonia

      it took you all the way to here before you ever told your reader anything about disease. Think about how you would want to think about a virus...

    1. 85 deaths per year in the United States caused by the disease. In recent years, however, this number has shrunk to about 8.

      denominators would help here

    2. The vaccines are not 100% effective, but in cases where vaccinated children do still contract the disease, it is half as contagious as it is when the virus infects unvaccinated children

      "although 90% of children in the US are vaccinated, the vaccine does not always protect from viral infection. If a vaccinated child is infected, however, the disease is much less severe".

    3. VZV does not have to be transmitted via direct contact, although contact with secretions from a person infected with VZV can result in infection. One of the primary ways that VZV is transmitted is through respiratory pathways.

      why not say, "VZV is transmitted through respiratory droplets, direct and indirect contact".

    4. specific place

      it's ok to say global and leave it at that. Why is it seasonal?

    5. enpox (which typically occurs in children), and shingles. Shingles can occur in adults who had chickenpox as children when the virus, which remained latent in the Dorsal Root Ganglia, becomes active again.

      in text citation. also, try to stay at the population level. DRGs are not global.

    6. Dorsal Root Ganglia until it is reactivated later in life and becomes Shingles.

      save for later

    7. t most are familiar with.

      you need to set this up a bit more

    8. ng the mucosa,

      In this section, try to use a more casual language. Something that explains the viral disease and prevalence. Things you might tell your aunt about.

    9. x and can reoccur later in adults as Shingles.

      lots of thoughts here. start with Chicken pox and tell me about the disease. You can bring shingles in later if you want to talk about reactivation.

    1. Vector

      remind your reader what the vector is...you don't have to use jargon here...mosquito is perfectly reasonable.

    2. fter a large surge in infections in 2012.

      I don't understand this sentence.

    3. euroinvasive diseases like encephalitis,

      or you can say, "rarely (1% of cases), WNV can invade the nervous system and cause inflammation (encephalitis)". Try to explain as much as you can and avoid using jargon.

    4. 94% of cases

      denominator please

    5. be transmitted through blood transfusions or organ transplants.

      put some numbers on this and in text citations please

    6. mosquito-bird-mosquito cycle

      a bit much in your first sentence. why not start with the disease...

    1. virus can be food- or water-borne, and it can survive on physical surfaces, which can lead to viral outbreaks in environments such as schools or cruise ships.2

      numbers here...

    1. Several laboratory tests, such as enzyme-linked immunosorbent assay (ELISA), can diagnose CCHFV by detecting specific molecules (antigens) or RNA sequences unique to the virus [

      Is this the only way to diagnose the disease? maybe talk about other diseases you might have to distinguish between and then bring up ELISA. Seems like you are solving a problem before you've explained that there is one.

    2. with mortality rates of up to 30% [1

      what's the denominator here?

    1. e 1: Lytic Cycle of a Virus

      you may want to draw your own picture...this isn't very good

    2. HSV-1 and HSV-2 can also go into periods of latency, meaning the virus is not actively being produced in the host (Nicoll, Proenca & Efstathiou, 2012). During latency, the host is absent of disease and no transmittance can occur (Nicoll, Proenca & Efstathiou, 2012). The host acts as a reservoir during latency and periodically the virus reactivates and the host can infect others (Nicoll, Proenca & Efstathiou, 2012). There are currently no vaccinations or prophylactic measures to completely prevent the spread of herpes (Akhtar & Shukla, 2009). The use of condoms and washing ones hands are effective methods to prevent the spread of herpes (“Herpes Simplex Virus”).

      you dipped into the molecular and then back out to general. watch your register here.

    3. HSV-1 and 2 binds to receptors on epithelial cells triggering the fusion with the cell (Karasneh & Shukla, 2011). Once inside the cell, viral DNA enters the nucleus and allows for viral transcription through the lytic cylce (Nicoll, Proenca & Efstathiou, 2012). The lytic cycle is the process in which viruses overtake cells and uses host machinery to reproduce and results in the killing of the host cell to release the virus to infect surrounding tissues (Figure 1)

      this may need to be elsewhere. It doesn't really fit with modes of transmission

    4. Genital and oral herpes is transmitted through skin-to-skin contact and mucous membrane contact with an infected individual (Nicoll, Proenca & Efstathiou, 2012). Herpes can be transmitted through sexual intercourse and kissing

      can you combine these two ideas?

    5. capsid and are surrounded in a lipid bilayer

      a picture would be helpful here.

    1. ffects as inflammation in the brain, blood disorders, eye infections, deafness, and others

      add numbers to all of your statements. It's too frightening otherwise.

    2. the CSF is produced (2). The virus then replicates within these areas and can penetrate into the brain and destroy some of the epithelial integrity, causing it to disintegrate into the CSF (2).

      this is also the same idea. maybe stick with the idea that the virus can get into the CSF and cause inflammation in the meninges and CNS. You are trying to take on too much information here and it is less than clear.

    3. re, leading to meningitis and encephalitis (

      same statement as the one above

    4. s, bleeding, fluid build-up, and the death of local exocrine and skin cells

      this sounds terrible but doesn't jive with the symptoms mentioned above.

    5. such as sports teams and classrooms

      you start off by saying it's not very prevalent in modern cultures but you only talk about US cases here.

    6. though research of the development and spread of the virus are primarily done through animal studies (2). MuV belongs to the family Paramyxoviridae. The virus is enclosed in a protein shell (2) and seven linked transcription units (2). It is infect healthy cells by fusing its membrane to the membrane of a target cell (2), and these infected cells are able to attach to other healthy cells to spread the infection (2).

      maybe save this until later.

    7. While mumps is a disease t

      why don't you describe the disease first?

    1. Regular contact with infected individuals such as hugging, kissing, sharing drinks and utensils, and shaking hands does not transmit the disease.

      please turn this sentence around do you emphasize the part where these are NOT likely transmission routes.

    2. riends of those infected (WHO, 2016).

      you may want to elaborate on these drugs a bit. Maybe how they work (once you've discussed replication).

    3. sever. T


    4. Disease Prevalence and Demographic

      please refer to your figures in your text so I know when to look at them.

    5. Figure 1: The path of HIV through the host cell. Source: Becerra et al. (2016)

      move this to later...it is too early.

    6. Once inside the body, the virus uses the host's cells by "hijacking the cell’s machinery" and replicating its own genomic material along with the DNA of the host (Becerra et al., 454).

      maybe put this later. stick to the global part here.

    1. Proteins DNM1/Dynamin 1 or DNM2/Dyamin 2 function to pinch the plasma membrane to enclose the virus in a Clathrin Coated Vesicle (CCV), and bring the CHIKV virus into the cytoplasm (Viralzone).

      this is a lot of molecular mechanism...you might get bogged down here. How about just saying endocytosis first and then if the clathrin comes in as part of uncoating, then bring it up. Much of this is classic cell biology that is not specific to the virus.

    2. ith mechanisms similar to that of other alphaviruses, with selectivity for receptors not found on all types of cells (Solignat et. al). CHIKV has demonstrated selectivity for proliferation in various cell types such as microphages, the kidney epithelial cell line (HEK-293T), the hepatocarcinoma epithelial line (HUH7), lung cells (MRC-5), skeletal muscle cells, and various endothelial cell lines (ThRBMEC and hCMEC/D3) (Solignat et. al).

      maybe relate how these types of cells may play a role in disease. Right now, it is a laundry list of cells that can be infected by CHIKV in the lab.

    3. as binding to receptors, on the host cell membrane (

      which receptors?

    4. he host cell and

      which cells? which host? just remind everyone

    5. Two structural proteins encoded by the CHIKV RNA strand, E1 and E2

      that's a lot of information...two structural proteins (what does that mean to you?) and RNA strand (means what?) and E1 and E2 (not very informative). Maybe start with the overall structure of the virus (capsid, etc), then you can work your way to E1 and E2.

    6. arboviruses

      I think this is the first time you mention this...maybe just say related viruses.

    7. skyrocketed

      can you put some numbers on skyrocket?

    8. veremic


    9. The Chikungunya virus itself is a type of Alphavirus (Weaver et. al, 1231), which are structurally characterized by having eighty trimeric glycoprotein spikes (1) which allow the virus entry into the host cell (Snyder and Mukhopadhyay) via promoting the fusion of viral and target host cell membranes (Yang et. al).

      save this for the life cycle part..it is jarring in this paragraph.

    1. Coxsackievirus contains various dips along it's virion surface in which the binding occurs. By doing so, instability occurs allows for a fatty acid to be released.

      I'm not sure what this means either. How does the virus attach? penetrate? uncoat? replicate? assemble? escape?

    2. Once attached to the receptor, the virus binds to it

      how is attached and bound different?

    3. external

      external to what? I'm not sure what this means.

    4. a high transmission rate in East and Southeast Asian countries. The most affected countries include Taiwan, Singapore, Vietnam, India and China (Mao). This disease tends to occur in areas with fluctuating cli

      give numbers and cite resouces

    5. opulation. It is a non zoonotic disease as it can not be transmitted to animals(CDC).

      wait...it is non-zoonotic because it can be transmitted to animals? I'm confused. generally, this classification is used to discuss transmission to humans from animals, not the other way around.

    6. categorized alongside p

      what does this mean? do you mean these are closely related viruses?

    1. The Yellow Fever Virus (YFV) is a flavivirus that is a member of a larger family of hemorrhagic fever viruses. YFV can cause characteristic yellowing (jaundice) of the whites of the eyes and skin due to damage in the liver cells. Spread by mosquitos, the virus has a 3-6 day incubation period with the first clinical signs appearing soon after. The first period’s signs include fever, vomiting, and muscle aches among other things. The second period is a remission period where a patient either experiences disappearance of initial symptoms or progresses to the third period, intoxication where the patient experiences continuing symptoms and can worsen to the point of death 7-10 days after initial onset of symptoms.

      include numbers for incidence and prevalence. Think about history of the virus be more specific about the viral course.

    1. low threat Zika fever itself ge

      can you give numbers to the cases that are of greater concern (percent infected or exposed)?

    2. Figure 1

      remember to cite your images at the image.

    3. s followed leading up to

      this is awkward....did the outbreaks follow or precede the most recent...

    1. , as mentioned earlier it is primarily symptom based, consisting of rest, fluid intake, platelet, or red blood cell transfusion, thus depending on the severity of the condition, and typically with a better prognosis and low risk of death if diagnosed early (1). In regards to how this virus is transmitted, it is done by getting bitten by the female Aedes aegypti o

      redundant. create a story that incorporates this information

    2. Viruses of the family flaviviridae are single stranded, positive, enveloped RNA viruses that are most commonly found in certain arthropod species, sometimes transferring over and infecting humans via bites or stings (6).Within the spectrum of Dengue Virus, it has been found that there are approximately 4 different serotypes (viral classification based on presence of certain antigens) called; DENV-1, DENV-2, DENV-3, and DENV-4 (1). In regards to the DENV structure; it is a 50nm virus enclosed in a lipid membrane with about 180 copies of envelope E protein attached to the surface of the membrane via transmembrane segment (1). The viral genome is about 11,000 bases, and consists of a polyprotein that is divided into three structural proteins, C, prM, E; seven nonstructural proteins, NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5, and short non-coding regions on both the 5’ and 3’ ends (1).

      this isn't about the disease...save for the molecular section

    3. As mentioned earlier, dengue virus is a type of virus that hails from a group of viruses that are from the the family flaviviridae. These types of viruses also include other similar type viruses such as West Nile, Yellow Fever and Zika viruses.

      redundant, put these together.

    4. The virus has a classification system that has been imposed by the World Health Organization (WHO) in 1974 in order to assist in its treatment and diagnosis, which has gone through revisions in the years 2009 and 2011, which classifies the disease’s severity as dengue fever, and dengue hemorrhagic fever grades 1-4 (3) The virus has a variety of symptoms with severities depending on its subtype. Typical symptoms of dengue fever include; joint pain, high fever, nausea, low white blood cell count, whereas the more severe version of dengue hemorrhagic fever entails

      how much of this is central to your point here?

    5. flavivirus

      please use the proper name, not the family name

    6. us is quite prevalent in t

      you don't need the qualifier if you have the numbers

    1. Herpes simplex virus can affect everyone all over the world and cause major life-threatening diseases.

      you jump between the global impacts and the virus life cycle. Separate them into two thoughts

    2. e herpes simplex virus can also cause mortality. Meningitis can result from HSV-2 (Engleberg). Also, HSV-1 can enter the central nervous system causing fatal encephalitis (Engleberg), or inflammation of the brain.

      hsv remains latent in the neurons....

    3. Americas, and the Western Pacific (WHO)


    4. Almost all humans have HSV-1, but the majority do not show symptoms (Engleberg). In fact, only about one third of people with the virus see symptoms (Engleberg). Globally, approximately 67% of people have HSV-1

      contradiction...almost all and 67% are different numbers. Make sure that you understand what "have HSV" means versus having infectious HSV.

    5. he treatment reduces symptoms, but does not prevent the infected person from having symptoms ever again.

      I would argue that you could talk more about the symptoms and treatment here. You are writing as if we all know what herpes looks like.

    6. HSV-1 affects the face and skin and HSV-2 affects the genital area

      these are general classifications. there is no reason what HSV-2 can't cause oral disease.

    1. Prevalence and Diagnosis

      you may be able to incorporate a number of these points into your basic overview.

    2. r over a long period of time,

      numbers please

    3. infected, further transmission of the virus is a result of contact from bodily fluids such as breast milk, blood, vomit, stool, urine, and others. (Mog

      how likely is that?

    4. ebola. (Center of D

      Ebola (ref). Don't put a period at the end of the sentence prior to your reference

    1. The virus encodes its genetic material in RNA and uses it to infect the host

      seems random in this train of thought

    2. The other clinical form of rabies, known as the numb type or the non-classical or paralytic type, is characterized by feelings of weakness or paralysis

      you brought this up and then don't give it the same treatment as classical. how is it passed, how is it different?

    3. nues to find improved methods of prevention and treatment.

      can you give some historical perspective to this numbers

    1. genetically engineered live attenuated human rotavirus strains or hybrid human-bovine reassortment rotavirus strains

      how is this relevant to your story? what are you trying to say here?

    2. Geographical Distribution

      make sure you cite your sources for your figure and refer to it in your text.

    3. diversity in strains o

      why is this important

    4. Common symptoms include vomiting, diarrhea, and fever for three to eight days. The incubation period for the virus is two days, and diagnosis is often executed by the detection of rotavirus antigen in stool samples

      maybe set this up as a timeline rather than a string of facts with times associated with them.

    5. of contaminated food or water.

      fecal oral is not different than ingestion of contaminated food

    6. so it is primarily transmitted via the fecal-oral route

      being contagious and stable doesn't mean it's transmitted through any particular route

    7. Rotavirus molecules are non enveloped and double-shelled, and have a similar appearance to that of a wheel.

      this is a bit too molecular for what follows and what comes before. save for later

    1. Global perspective on the virus would be the disease it causes, the prevalence, mortality, vaccine, etc. You need to set up why this is important well before you launch into the molecular mechanisms of the virus.

    2. The integration of viral DNA into normal host DNA is only a factor with High Risk-HPV (2). HPV integrates into double stranded breaks in the DNA structure caused by oxidative molecules or HPV proteins (2). HPV then uses the DNA damage repair system for it’s own amplification by disrupting cell cycle checkpoints and eliminating factors that cause cell apoptosis (2). Also, HPV’s use of episomal DNA may give it a larger number of DNA fragments that can be inserted in host DNA (2). Integrating is also mediated by tethering of the viral DNA to the host DNA by a protein called Bromodomain protein 4 (Brd4). This viral integration into host DNA is linked to genomic instability, a major hallmark of cancer (2).

      also save...too much too soon

    3. High risk HPV’s or HR-HPV’s are the genotypes associated with malignancy and high-grade dysplasias which are abnormal cell growths that precede cervical cancer (1,2). Both high risk and low risk infections begin with the HPV virus passing an epithelial barrier and infecting the basal epithelial cells at the squamous columnar junction (2). The virus enters the epithelial cell via a receptor called Heparan sulfate proteoglycans receptor (HSPG) and its coreceptors alpha 6 integrin and laminin 5, which sense when adhesion has occurred (2). The virus is then endocytosed and enters the nucleus through breaks in the nuclear membrane (2). The viruses localizes a transcriptionally active region of the nucleus called the ND10 bodies (2). The viral DNA replicates at very low levels in a structure called an episome, which replicates independently of host chromosomal DNA (1,2). When the host cell undergoes differentiation to become a non-replicating barrier cell, the viral DNA switches its mode of replication to a method that allows for amplification (2). The L1 and L2 proteins are expressed, allowing the creation of the necessary capsid proteins for viral assembly (2). Virions are then sloughed off as epithelial cells are sloughed off in normal epithelial wear and tear for further transmission (2). Papillomavirus changes in epithelium may take months to show up, but when they do, they often form a bump on the skin or mucous membrane (1).

      save this for the molecular part

    4. immunocompromised

      ummmm...are you sure that you want to make this statement? You do not have to be immunocompromised to have warts on your hands....simply a breach in the skin barrier and high enough viral innoculum.

    5. ordinary

      nobody is ordinary....

    6. tiny amounts of HPV

      trace? tiny implies small in size, not few in number

    7. to cause infection

      maybe explain where warts would be normally and ease into sex. you went right for sex but most people would associate warts with hands, etc.

    8. The particles of these viruses are produced by two proteins that are close together called L1 and L2 proteins, which contain a small circular genome (1). The L1 and L2 encode for the capsid proteins, or the outer protein shell of the virus (2). The proteins E1 and E2 are responsible for viral transcription (2). There are 150 HPV genotypes and each is typically associated with a particular region of the body or epithelium (1)

      save this for the molecular stuff. You are switching tone and register all over the place here.

    1. Vaccination Efforts


    2. e of HCV Infection Throughout the World.

      refer to the figure rather than repeat all the data in the text. Just point out that developing countries are more hard hit than developed.

    3. Schistosomiasis is a water-borne parasite typically acquired by ingesting or bathing in contaminated water sources, and is most common in Egypt (Frank 41). As a result, a treatment used to cure the presence of the parasites in the blood stream, called parenteral antischistosomal therapy (PAT), was common practice in this area from 1950s-1980s (Frank 41). Unfortunately the protocol used in administering this treatment involved reusing needles and insufficient decontamination, leading to widespread HCV infection

      cool story but set it up. You could write something like, "paradoxicallly, the cure for another disease actually increased the rate of HCV" then you can launch into your story about Schisto.

    4. f a blood presence in the water sources

      what does a "blood presence" mean. Do you mean to say that the water is contaminated with HCV-infected human blood? eeewww. but you didn't make that very clear.

    5. roportionally lower rates o

      maybe say where things are highest first and give appropriate numbers.

    6. previously discussed

      don't make your reader go back looking for something you've already said, just say it again.

    7. Prevalence has also been shown to vary among age groups

      Paralell structure....stay with risk factors

    8. ss developed countries who have yet to implement these screening procedures continue to have higher rates of transmission

      how much higher? be specific because the real numbers are more compelling than "higher" and "decrease"

    9. ecrease the frequenc