administration of either antibiotics or probiotics to, respectively, increase or decrease microbial numbers and diversity

Our Gut Microbes Strongly Influence Our Emotional Behaviors

Gram positive stain

Epidemiology

Disease: Signs and Symptoms

cell surface

symptomatically

luctuating climates

recently

transmission

The initial symptoms o

Enterovirus genus

categorized alongside poliovirus

ers into the cell's cytosol.

RME

Caroline Beuligmann

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).

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

a (See Figure 1 and Table 2)

released via budding.

hree proteins—P, V, and C.

Life cycle of the measles virus

lipid rafts

peplomers

see figure 1

Structure

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).

Mastomys natalensis

e Lassa virus

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

animal borne

the first to die from the disease.

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

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.

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

at can grow in the gut of

attenuated

positive stain of Poliovirus

reduced the polio cases.

pe 1 and 3 are currently foun

paralysis.

quire their envelope

psids bud into the ER lumen.

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.

While research into the

tory drugs are the only treatment, since no

re severe respiratory problems

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

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).

viral respiratory disease

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

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).

help them fight off infection

The Lymphocytic Choriomeningitis Virus (LCMV)

The spread of smallpox has decreased dramatically.

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

f symptoms that are general enough

creates a localized pus-filled rash.

making it highly contagious.

s variola.

of smallpox i

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

family and functions as effectively as cowpox.

vaccinia

vaccinated. T

effective process for smallpox was confirmed,

ollowing with smallpox r

o get vaccinated out of fear.

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.

vaccination for smallpox decreased significantly in the early 1980s.

h high mortality and contagious levels, fi

incredibly

onomic and sanitary conditions

r

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

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.

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).

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

EBV causes infectious mononucleosis (mono) a

viral

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

zoonotic

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

-2 is less detecte

causing lower respiratory diseases.

36% of all reported cases r

. 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).

lation of aerosolized mouse droppings.

ot spread from person to person.

o several Native American Tribes.

four corners

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.

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

the deer mouse was the primary carrier of the virus

re was an outbreak in the southw

rdiopulmonary Syndrome in humans

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).

AdV antibodies in their bodies, i

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

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

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

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.

specific place

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.

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

t most are familiar with.

ng the mucosa,

x and can reoccur later in adults as Shingles.

Vector

fter a large surge in infections in 2012.

euroinvasive diseases like encephalitis,

94% of cases

be transmitted through blood transfusions or organ transplants.

mosquito-bird-mosquito cycle

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

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 [

with mortality rates of up to 30% [1

e 1: Lytic Cycle of a Virus

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”).

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)

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

capsid and are surrounded in a lipid bilayer

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

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).

re, leading to meningitis and encephalitis (

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

such as sports teams and classrooms

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).

While mumps is a disease t

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

riends of those infected (WHO, 2016).

sever. T

Disease Prevalence and Demographic

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

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).

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).

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).

as binding to receptors, on the host cell membrane (

he host cell and

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

arboviruses

skyrocketed

veremic

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).

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.

Once attached to the receptor, the virus binds to it

external

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

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

categorized alongside p

personalized therapy with macrophages

macrophages (viruses of bacteria)

between September to April.

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.

low threat Zika fever itself ge

Figure 1

s followed leading up to

, 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

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).

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.

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

flavivirus

us is quite prevalent in t

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

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.

Americas, and the Western Pacific (WHO)

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

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

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

Prevalence and Diagnosis

r over a long period of time,

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

ebola. (Center of D

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

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

nues to find improved methods of prevention and treatment.

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

Geographical Distribution

diversity in strains o

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

of contaminated food or water.

so it is primarily transmitted via the fecal-oral route

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

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).

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).

immunocompromised

ordinary

tiny amounts of HPV

to cause infection

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)

Vaccination Efforts

e of HCV Infection Throughout the World.

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

f a blood presence in the water sources

roportionally lower rates o

previously discussed

Prevalence has also been shown to vary among age groups

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

ecrease the frequenc