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253 Cards in this Set

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Is a virus living?
Yes in the sense that it has DNA or RNA

No in the sense that it lacks the ability to generate ATP and other biosynthetic machinery (ex: ribosome) needed to carry out protein synthesis.

Virus= Obligate Intracellular Parasite
T or F
A virus genome consists of either DNA or RNA but never both?
True!
It can have one or the other.

Variety of options- nucleic acid can be linear, circular, ds, ss, segmented, or non semgented.
Describe the general structure of a virus.
Nucleic acid contained within CAPSID which is made up of protein molecules called CAPSOMERES.

The entire structure is called a Nucleocapsid. Has a distinctive symmetry.
What are the different shapes a virus coat can take on?

Why is it so important to be symmetrical?
Icosahedral (12 vertices, 20 faces)
Helical
Complex (Pox virus)

Important to be symmetrical because viruses are constantly assembling and disassembling.
T or F
Naked viruses are more fragile and less stable in the environment than viruses that have an envelope coat?
False!

Enveloped viruses have fragile lipid bilayer coat that makes them more susceptible to alcohol, low PH, etc. The "Naked viruses" have a more protective nucleocapsid.
What are the functions of a nucleocapsid?
1. packaging and protecting nucleic acid

2. transport of nucleic acid from cell to cell

3. promote viral attachment to target cell receptors
T or F
DNA viruses can be icosahedral and/or helical?
False
DNA viruses are NEVER Helical!
Give an example of a double-stranded DNA virus that is enveloped.
Herpesvirus
In terms of the "Adenovirus" is it:
DNA or RNA
double stranded or single stranded
enveloped or naked
linear or circular nucleic acid
Adenovirus= DNA, double stranded, naked (non-enveloped), Linear
Name a complex, enveloped DNA virus?
The only one is POXVIRIDAE (Poxvirus)
In terms of "Papovaviridae" (Papilloma + Polyomavirus), is it:
DNA or RNA
double stranded or single stranded
enveloped or naked
Papilloma + Polyomavirus=

DNA, doube stranded, naked (non-enveloped), Circular
Name a DNA virus that is single stranded and non-enveloped?
Parvoviridae
In terms of adhering to a cell's membrane, receptor molecules for viruses vary, but they are typically...
Glycoproteins (from the viral envelopes or capsids)
What is meant by "Host range"?

What is a virus that has a broad host range? What is one that has a narrow host range?
The kinds of cells, tissues, and species that a virus can infect.

Broad = HSV = infects lots of different species and tissues

Narrow = HPV = infects only humans and epithelial cells
What is "tissue tropism"?
The types of cells a virus can infect.

ex: some viruses like Hepatitis have a narrow tissue tropism (primarily affect liver tissue).
T or F
The presence or absence of certain receptors determines the number of species, tissues, and cells a virus can bind to.
True!

Receptors determine Host Range as well as Tissue tropism.
What are three mechanisms of Penetration (Entry) of a virus into the cell? Which is(are) most common?
1. Direct Penetration
2. Membrane fusion *
3. Receptor-mediated endocytosis *

* = most common
Describe the process of "Membrane Fusion" that a virus uses to enter a cell.
Typically enveloped viruses with glycoprotein spikes will attach to receptors on cell. The two membranes will fuse. The nucleocapsid will be released into cytoplasm.

*fusion at the neutral pH of extracellular environment
Describe the process of "Receptor-mediated endocytosis" that a virus uses to enter a cell.
Virus will be enclosed in an endosome that has a low pH. The low pH leads to fusion and bursting open of nuclear envelope/capsule which releases nucleocapsid.
What is "viropexis"?
Another name for Receptor-mediated endocytosis that some viruses use to enter cell.
All DNA virus genomes will repicate in the ___. (Exception?)

All RNA virus genomes will replicate in the ___. (Exception?)
DNA = nucleus (because they can use the cell's machinery). Exception is Poxvirus

RNA= cytoplasm (typically come with own machinery). Exception is Influenza.
All viruses need to get to what stage in order to replicate (i.e. what must they produce)?
mRNA

This will allow them to translate their genes into protein.
What does DNA-dependent RNA polymerase do? Is it found in the host cell or virus?
It makes RNA from DNA (specifically mRNA).

Found in the Host cell.
What does RNA-dependent RNA polymerase do? Is it found in the host cell or virus?
Makes RNA from an RNA template. Eukaryotic cells don't have this capacity so viruses must bring it along.

Found in the Virus.
T or F

ssRNA+ viruses (or ssRNA of positive polarity) upon entering the cell, will replicate within the cytoplasm?
True

ssRNA+ viruses have genomes identical to mRNA. Thus they can immediately make protein (no need for transcription). They do so on the ribosomes in the cytoplasm.
Why are larger viruses more susceptible to antiviral chemotherapy?
They are less dependent on host cell function and encode more of their own proteins which means more targets for drugs.
What defines whether a viral gene that is transcribed within a host is "Early" or "Late"?
Early means BEFORE replication of DNA.

Late means AFTER replication of DNA. Usually from the newly synthesized viral genomes.
What do Early genes encode? What do Late genes encode?
Early genes: typically proteins that help with DNA replication.

Late genes: typically structural proteins that are incorporated into progeny virus.
How are naked viruses released from the cell?
Because the viron is completed after assembly (no envelope), the host cell simply lyses and released the virus.
How are enveloped viruses released from the cell?
They must acquire an envelope first. They are guided to the membrane by MI "matrix protein" and they incorporate their viral glycoproteins into the cell membrane. Then they bud out.

* The viral glycoproteins that are inserted into plasma membrane generate are the antigens of viruses!
What determines when budding of virus stops?
When the host cell dies from loss of membrane integrity.
What does Cytopathic effect (CPE) refer to?
The cellular changes that are induced by a virus and are visible by light microscopy.
Viruses, such as the cytomegalovirus, that can cause characteristic nulcear inclusion bodies are made up of what type of genome?
Nuclear = DNA virus
What is a "syncytia"?
A giant multi-nucleated cell formed by the fusion of neighboring cells.

ex: Herpesvirus
What type of virus produces the classic cytoplasmic inclusion called the "negri body"?
Cytoplasmic = RNA virus

Rabies virus
What are the three different types of temporal profiles a viral infection can take?

Give an example of a virus that does each.
1. Acute...influenza
2. Latent...Herpes virus
3. Chronic...HIV
What is the definition of a Latent infection?
Once virus enters cell, it will hide and NO VIRAL PARTICLES WILL BE MADE. It is a quiescent state.
What is meant by "secondary viremia" with regards to viruses?
"primary viremia" is when the virus initially enters the blood stream and lymph from the site of infection and spreads to tissues.

vs. "secondary viremia" which is when the virus RE-ENTERS the blood stream and can spread to more tissues.
Provide an example of a virus that enters the body via the following route of transmission:

-Respiratory/ Droplet
- Ingestion/Fecal-Oral
- Direct Skin contact
- Blood
- Zoonosis
- Sexual Contact
- Transplacental
- Respiratory = Influenza (enveloped)
- GI = Rotavirus (no envelope)
- Contact = Herpes Virus, Poxvirus
- Blood = HIV, Hep C
- Zoonosis= Rabies
- Sexual Contact = HPV, Hep B
- Transplacental = Herpes , Parvovirus B19
What the hallmark of all herpesviruses?
It can establish LATENCY within the host.

i.e. quiescent, nonreplicating state from which viruses can be subsequently reactivated.
What is the shape of the Herpes virus, is it encapsulated, and what type of DNA does it have?
Icosahedral symmetry
Enveloped
linear, dsDNA
What is unique about the coat of the Herpes Virus family?
It has a Tegument aka. extra, amorphous protein layer covering capsid

(F) contains proteins to help hijack hosts proteins and divert host proliferation
Why does HSV primarily get transmitted through a moist environment (ex: sexual or direct contact)?
Because it has an envelope (thus fragile and prefers moist membranes).

They also tend to stay at the site of entry.
Describe the replication of HSV.
"Cascade control" aka sequential steps in transcription

** 1. Immediate early proteins- Hijacking proteins are transcribed in nucleus and then translated in cytoplasm using Host cell's enzymes and machinery

2. Early proteins- for DNA synthesis made. They make a lot of their own machinery and replicate DNA.

3. Late proteins- structural proteins (capsid, glycoprotein) are made
Why do lesions of HSV tend to coalesce and only locally spread?
Tend to spread Cell-to- Cell.

The viruses, once they bud, can actually attach to adjacent cells and form multinucleated-giant cell syncytia.
T or F

Site of Latency is related to where a Herpesvirus originally infected the body.
True

Site of latency is related to Site of initial infection (Herpes, remember, spreads locally)
What family of viruses is the largest and most genetically complex of the known viruses?
Poxvirus (complex coat, DNA, enveloped)
What is a zoonotic infection that caused local disease on the hands of milkmaids?
Cowpox

Poxviridae family
What is an "orf virus"?
A poxvirus of sheep and goats which can accidentally infect humans.
Why was the extinction of Smallpox possible?
1. Humans are only hosts.
2. Virus doesn't remain latent, so if you survive, there is life-long immunity.
3. There were no asymptomatic cases.
4. Time, money, effort was put into erradication.
What is the characteristic morphology of Poxviruses (i.e. how do they look under a microscope)?
- overall shape is oval/brick-shaped

-within the virus, the core looks like dumbell because of large lateral bodies pressing down
What are "Guarnieri's bodies"?
Inclusion bodies where virus is assembled (in the cytoplasm-remember-because it's unique!)
Describe the pathogenesis of small pox (how the variola virus enters and how it spreads).
Virus enters respiratory tract and replicates > Infects macrophages which carry it to lymph nodes > replicates and spreads through blood and lymph (viremia)

"Pox" = hemorrhage of small vessels of dermis
How do you distinguish smallpox (variola) from chicken pox (varicella)?
Smallpox- the skin pox all turn up at the same time and look the same

Chicken pox- there may be a succession of lesions. one might be scabbing, another is just forming, etc.
What is "molluscum contagiosum"?
It is a virus that belongs to the Poxvirus family. Humans are the sole reservoir and it's acquired via direct contact.

Replicates in cytoplasm and forms an inclusion is called a "Molluscum body"
A distraught medical student comes to your office. He complains that he had cold sores around his mouth several months ago and they went away by themselves. Every time, around his exams, they keep returning in the exact same spot! He can't seem to understand why they keep cropping up in the same area.

What do you tell him?
The HSV infects mucosal epithelial cells (primary site of infection) and then will go into a period of latency. It will crawl up an adjacent neuron (retrograde transport) and hide there for a while. Stress (exams) tends to reactivate it and it crawl back down to the same area and starts to shed.
There are >100 serotypes of the Adenovirus. What determines the serotype?
Serotype is mainly a result of differences in penton base and fiber protein (determine nature of tissue tropism and disease).
Why do adenoviruses cause gastrointestinal infections?
Because they are naked (no envelope) and can thus with-stand the acid of the stomach. They can be transmitted via feco-oral route.
What is "swimming pool conjunctivits"?
It is conjunctivits caused by Adenovirus which, because it lacks an envelope, is capable of surviving chlorinated pools.
What are the three types of viral infections that an adenovirus can develop within a cell?
1. Lytic
2. Latent
3. oncogenic transformation *
What are the two subfamilies of the Papovavirus?
Papillomavirus (HPV)

Polyomavirus (JC and BK viruses)
What diseases can the JC and BK viruses cause and in what types of individuals?
Immunocompromised individuals (ex: HIV patients) can get diseases.

JC => PML (progressive multifocal leukoencephalopathy)

BK => renal disease
What is the size of the Papillomavirus and the shape of it's genome?

What are E6 and E7?
Small! 8 kb, CIRCULAR genome

E6 and E7 are particular early genes that are capable of disrupting tumor suppressor genes (p53 and rb), if they integrate into the host genome.
How is HPV acquired and how is this related to one of its principle clinical symptoms?
Acquired via casual contact (epithelium on skin, throat, cervix).

It thus forms WARTS (extensive proliferation of keratinocytes-hyperkeratinosis- that forms thick, cornified layer of dead cells containing viral progeny)
Why do warts sometimes disappear and reappear in the same spot after some time?
The HPV will reach the basement membrane of skin and hitch a ride on the keratinocytes (using their machinery to proliferate). Many viral progeny are in the warts themselves, but some virual particles can remain in basal stem cells and lay low (QUIET) for some time.
What strand of HPV virus tend to cause anogenital warts?
HPV-6 and HPV-11
What is the smallest DNA virus?
Parvovirus
T or F
Multiple members of the Parvovirus family can cause human disease.
False

only B19 strain causes human disease.
What type of cells do parvoviruses tend to infect?

What clinical symptom is associated with Parvovirus?
Rapidly dividing cells (like RBCs, another name for the virus is erythrovirus)

Because it hijacks RBCs, it can cause an erythematous rash (FIFTH DISEASE)
What are the five common childhood exanthems or skin rashes?
1. Varicella
2. Rubella
3. Roseola
4. Measles
5. Fifth Disease (hence the name!)
What are the three major subfamilies of Herpesvirus and what distinguishes them?
Alphaherpesvirus (HSV, VZV)- neurons
Betaherpesvirus (CMV, HHV)- lymphocytes
Gammaherpesvirus (EBV, KSHV)

Surface glycoproteins are distinct for each virus
What are the four key structural components of the Herpesvirus?
1. Outer envelope
2. Tegument
3. Nucleocapsid (Icosahedral)
4. Inner core (linear dsDNA)
What is the "tegument"?
It is an amorphous protein layer that lies between the outer envelope and nucleocapsid. UNIQUE to Herpesvirus! It helps tether envelope to capsid and assists in the replication process.
What characteristic finding would be present on a pathology slide identifying Herpesvirus?
Multinucleated giant cells with intranuclear inclusion bodies.
T of F
In terms of Herpes Virus, Transmission is typically asymptomatic with the exception of Varicella Zoster.
True

Asymptomatic transmission is the norm except for VZV
What is the primary mode of transmission of HSV-1 and HSV-2?
Person-to-person (direct contact)

Oral-Oral
Oral-genital
Genital-genital
Mother-child
T or F
90% of adults have been exposed to HSV-1 at some point?
True!

90% of adults (and 60% of children) have antibodies to HSV-1
What are some mucocutaneous manifestations of HSV-1 and HSV-2?

Genital herpes are most common in which strain?
Painful, oral lesions
Herpetic whitlow (skin infection from biting finger/nail)
Herpes Gladitorum (among wrestlers, lesion on face, neck, and arm)
Genital lesions (HSV-2 >> HSV-1)
What are some central nervous system diseases that arise from HSV-1 or HSV-2 infection?
Encephalitis- localized to temporal lobe
Benign meningitis
Bell's palsy (Cranial N. VII, facial droop)
Transverse myelitis (spinal cord inflammation)
What is TORCHES?

How does this help us determine whether women should have C-section or vaginal birth?
TORCHES = mnemonic for maternally transmitted infections (C= CMV, H= Herpes)

This lets us know that a pregnant mother with active herpes lesions is an indication for Cesarean section!

T= toxoplasmosis, O= other infections such as Parvo, HIV, Hep B, Cocksakie, R= rubella, S= syphilis
What is the #1 cause of corneal blindness in the US and what virus is it caused by?
Keratoconjunctivitis (dendritic ulcers that can scar over)

caused by Herpesvirus
How is Varicella spread?

What painful condition does the reactivation of VZV result in?
Transmitted via aerosol particles and direct contact (with pox lesions).

Shingles (Zoster)
How does Chicken Pox (VZV) look clinically and how can we distinguish it from smallpox?
"Dew drops on a rose petal" (pruritic vessels on erythematous base)

Unlike smallpox in which all vesicles are activated at once, in Chicken pox, the lesions can be seen at different stages of development.
Where does the VZV virus remain latent?

How can you tell that a rash is due to VZV reactivation rather than another disseminated infection?
DRG (dorsal root ganglion)

VZV = rash doesn't cross midline. It stays in its dermatomal distribution.

Disseminated infection = disseminated rash
What is Ramsay-Hunt syndrome?
An Herpes Zoster infection that affects the distribution of the FACIAL NERVE!

Usually results from DRG reactivation of a latent Herpes virus. Bells palsy, ear infection and palate and tongue lesions.
T or F

The administration of a zoster vaccine to older persons may prevent zoster (shingles) occurrence?
True

VZV-specific memory T cells decline with age so if you administer a vaccine to boost the T cells, you will be able to prevent Zoster from manifesting.
At what stage of life do the majority of CMV (cytomegalovirus) infections occur?
Early (within 1st year of life)

Transmission can occur in utero (remember TORCHES!)
T or F

The majority of CMV cases are asymptomatic, except in immunocompromised patients in which they can produce severe disease?
True

Can cause end organ disease, retinitis, esophagitis, pneumonitis etc. in transplant patients and AIDS patients.
If a baby comes to you in clinic who is born underweight, is microcephalic and has intracerebral calcifications on MRI, what viral cause might you look for?
CMV (one of the TORCHES)
What is the tissue trophism for CMV (i.e. what cells/tissues does it like to infect)?
Polys (neutrophils) and Lymphocytes

*Histologically looks like multinucleated giant cells with intranuclear inclusion bodies called "Owl-eye" inclusions
The major clinical syndrome associated with EBV is...?

What does it look like clinically
infectious mononucleosis

Associated with fever, exudative pharyngitis, lymphadenopathy, and splenomegaly. Also fatigue (the sleeping sickness).
What malignancies is EBV implicated in?
African Burkitt's lymphoma
Nasopharyngeal carcinoma
Post-transplant lymphoproliferative disorders
Primary CNS lymphoma
Cells infected by EBV express what protein on their surface?

(Bonus- what are Hodgkins lymphoma cells called?)
Latent Membrane Protein 2 = associated with cells infected by EBV


Hodgkin's lymphoma cells = Reed-Sternberg cells
T or F

Up to 95% of older children and adults have evidence of past infection of HHV-6 and HHV-7?
True

scary! mostly transmission through maternal saliva
What clinical condition is associated with HHV-6 and HHV-7 infection?
Sixth disease (Roseola infantum)

high fever, Upper respiratory symptoms, lymphadenopathy, fine maculopapular rash (sandpaper type)
What is unique about the latency period of HHV-6?
It is able to integrate it's genome into the chromosome of hosts.
What is the tissue tropism of HHV-6?

What is the tissue tropism of HHV-7?
HHV-6: T cells, monocytes, macrophages, etc.

HHV-7: specifically CD4+ T cells! (it can down regulate CD4 receptor expression)
What virus is associated with Kaposi's sarcoma?

What does Kaposi's sarcoma look like?
HHV-8

Painless vascular tumor of skin or mucous membranes. Associated with immunosuppression. Disease can have mass effect and be disfiguring (which is the primary problem, not painful).
Aside from the obvious Kaposi Sarcoma, what other clinical conditions might HHV 8 cause?
Primary effusion lymphoma (aggressive B cell lymphoma orginating from body cavities)

Castleman's disease: angiofollicular lymph node hyperplasia

Primary Pulmonary Hypertension?
What DNA virus is benign in monkeys but fatal in humans, progressing from an ulcer to hemorrhagic encephalitis?
Herpes B Virus
Why are negative stranded RNA viruses not immediately infective?
Because eukaryotic cells do not posses the RNA-dependent-RNA transcriptase needed to transcribe their genome, they need to bring it into the cell with them. This is additional step so they are not immediately infective.
What are the three serotypes of the Orthomyxovirus?

Which is (are) the most infectious?

Which have an animal reservoir?
Influenza A*
Influenza B*
Influenza C

Type A has an animal reservoir (H1N1 for instance is type A)
What is "Antigenic drift" (with reference to Orthomixoviruses)?
Point mutations arise in HA (Hemagglutin) and NA (Neuraminidase) genes. Associated with all 3 serotypes.

*This is what lead to variations in influenza virus from year to year.
What is "Antigenic Shift" (with reference to Orthomixoviruses)?
Reassortment of genome because a cell becomes doubly infected. Leads to emergence of new viruses (severe flu pandemics). Ex: Swine Flu
T or F

Antigenic shift happens in both Type A and B influenza.
False

Only type A can undergo antigenic shift. This is because it has an animal reservoir which facilitates the mixing of the genome.
What specifically about the Influenza virus facilitates the development of new strains (why do we get new epidemics and pandemics once in a while)?
Because it has a SEGMENTED genome, meaning it is capable of mutating and re-assorting gene segments, each which codes for 1 mRNA.

* Exhibits GENETIC INSTABILITY
What is the tissue tropism of Influenza viruses?

Why?
They tend to infect respiratory epithelium (transmitted through aerosols).

1) they need to bind to sialic acid receptors on the epithelium
2) HA glycoprotein has to be cleaved by host cell serine proteases which are only found in respiratory tract, to allow for fusion.
Why can influenza virus lead to more serious secondary bacterial side effects (pneumonia, etc.)?

Hint: think about what it's doing pathogenically.
1) It creates gaps in the respiratory epithelium that allows access to secondary pathogens and bacteria

2) It destroys cilia on surface of epithelium reducing clearance of infected mucous.
What is the structure of the Influenza virus:
envelope or naked?
segmented or non-segmented?
DNA or RNA?
ss or ds?
where does it replicate?
Enveloped
Segmented
Negative-stranded RNA genome
Replicates in nucleus (due to cap snatching)

* Pleomorphic (can take up several shapes!)
What two orthomixoviral proteins are the most important determinants of influenza virus virulence?

What does each do?
HA (Hemagglutin) and NA (Neuraminidase).

HA- involved in attachment of virus to sialic acid residues AND membrane fusion

NA- hydrolyze sialic acid so that virus can diffuse away from cell. It is also involved in PENETRATION of the mucus layer in respiratory tract.
What does each Influenza virus nucleocapsid segment contain?
viral RNA and 4 proteins:

1) NP- major nucleocapsid protein
2) PA, PB1, PB2= special viral RNA polymerase (it's buddy)
3) M1 (matrix protein)
4) M2 (pH activated ion channel)
What is the role of M1 matrix protein?

What is the role of M2 protein?
It promotes assembly and budding (guides the nucleocapsid in the process of budding)

M2 Ion channel- pH dependent ion channel which introduces more H+ into endosome to fuse viral envelope with endosomal membrane and release the viral genome.
Why does Influenza virus need to be replicated within the nucleus?

Is this the exception or the rule to RNA viruses?
Cap Snatching!

It lacks 5' capping activity which needs to be done in order to translate the mRNA into protein.

Thus it enters nucleus and "snatches" newly synthesized caps from eukaryotic mRNAs, attaches it to it's 5' end and returns to the cytosol to translate into viral proteins.

This is the EXCEPTION to the RNA virus rule.
Why is Neuraminidase (NA) glycoprotein a good target for Influenzaa drugs?
It cleaves sialic acid which releases virus into periphery. Without this, virus will not be able to be released and spread.
Amantadine and Rimantadine are anti-influenza drugs that target what?
M2 ion channel protein (prevent release of virus once within endosome)
Are Paramyxoviruses segmented or non segmented?

Are they genetically stable or unstable?
Non-segmented thus genetically stable

Remember this by thinking about Mumps- only one type of mumps.
Through what route are Paramyxoviruses transmitted?
Respiratory droplet (primary respiratory pathogens)

ex: respiratory secretions (sneezing, coughing)
What are the two major subfamilies of the Paramyxoviruses?

What major conditions are they responsible for?
Paramyxovirus (parainfluenza and measles and mumps, two major childhood illnesses)

Pneumovirus (RSV- respiratory syncytial virus, can cause bronchiolitis and pneumonia)
What surface protein distinguishes different members of the Paramyxovirus family?
The viral attachment protein (large glycoprotein) HN, H, or G

ex: G- RSV, H- Measles, HN- parainfluenza and mumps
What viral family does Mumps belong to? What is it's clinical manifestation?
Paramyxovirus (specifically Rubulavirus).

It is a nonpurulent infection of the salivary glands, specifically parotid. Typically benign and self-limiting.
What virus causes Measels aka Rubeola?
Paramyxovirus
What causes the classic maculopapular measles rash?
The T cells target the infected endothelial cells lining blood vessels. This results in a rash.
What clinical symptoms characterize Measles?
First KOPLIK's spots appear (red spot with bluish-whitish specks in center) in the oral mucosa.

Then the rash appears and spreads throughout body. Typically accompanied with fever.
What surface protein distinguishes different members of the Paramyxovirus family?
The viral attachment protein (large glycoprotein) HN, H, or G

ex: G- RSV, H- Measles, HN- parainfluenza and mumps
What virus causes Mumps? What is it's clinical manifestation?
Paramyxovirus (specifically Rubulavirus).

It is a nonpurulent infection of the salivary glands, specifically parotid. Typically benign and self-limiting.
What virus causes Measels aka Rubeola?
Paramyxovirus
What is responsible for the classic maculopapular measles rash?
The T cells target the infected endothelial cells lining blood vessels. This results in a rash.
What clinical symptoms characterize Measles?
First KOPLIK's spots appear (red spot with bluish-whitish specks in center) in the oral mucosa.

Then the rash appears and spreads throughout body. Typically accompanied with fever.
T or F

The Measles virus requires NA (neuroaminidase) activity?
FALSE!

The Measles virus does NOT use a sialic acid receptor! It has a CD46 glycoprotein receptor!
What is the classic shape of the Rhabdovirus (aka Rabies virus)? What is the shape of it's nucleocapsid?
Bullet shaped, helical nucleocapsid.
What characteristic finding is seen in say, a muscle biopsy of a patient infected with rabies?
Special eosinophilic (pink) cytoplasmic inclusion bodies = "Negri body"

Why cytoplasmic? because it's an RNA virus! replicates in cytoplasm.
Which is better: being bitten by a rabid animal on the ankle or on the neck?
The ankle! because the infection can spread through neurons and by the time it gets to the brain, it results in a pretty much incurable diffuse encephalitis.
Why do rabid animals (and humans for that matter) foam at the mouth?

Why are rabid animals "afraid" of water?
1. infection of the parotid gland (increased salivation)

2. It's not that they are afraid, it's just that they have difficulty swallowing because of CNS symptoms.
Why are people who are already bitten by a suspicious rabid bat (or exposed to one) given a regimen of vaccines against it?
Because rabies virus takes some time to replicate and spread, there is a window of opportunity to generate antibodies that will launch an immune response and prevent viremia.
T or F

If a patient has Pharyngitis, it is possible to distinguish viral pharyngitis from bacterial pharyngitis.
False

Viral pharyngitis can NOT be distinguished from bacterial pharyngitis on clinical grounds. (need to do a throat culture)
What is the most common viral etiology for the common cold?
Rhinovirus (30-50% of colds, all seasons)

second most common= Coronavirus
Why does viremia not occur with Rhinovirus?
Because it does not spread to sites outside the respiratory tract (i.e. you don't get it in the bloodstream). It likes the colder temperatures of the Upper Respiratory Tract.
Describe how the "common cold" produces symptoms such as cough, rhinorrhea, and stuffy nose.
Infection through inhalation (nasal cells) > irritation of airway receptors > bronchospasm/cough

Infection of cells > chemical mediators released > edema of tissues > nasal obstruction (clogging)

Infection of cells > inflammatory cells and mediators increase > increased mucous production > rhinorrhea (runny nose)
Why is it impossible to make a vaccine against the common cold?
There is incredible serological diversity (i.e. many subtypes) in Rhinovirus.

Rhinovirus also only accounts for 50% of colds, others include Coronavirus and Influenza, etc.
What virus causes Croup?
Almost all cases are caused by Parainfluenza virus (from Paramyxovirus family)
Why does infection by parainfluenza virus cause laryngotracheobronchitis in kids but only larynigitis in adults?
Adults have larger airways than children, so the edema that occurs will not constrict their airway to the extent of what happens in children.

*recall, tracheal rings are rigid, so mucous membrane swelling pushes inwards, narrowing the lumen
What are treatments for Croup?
Generally supportive care.
You can also use oral steroids (reduce inflammation) and inhaled epinephrine (smooth muscle relaxation)
What is the difference between an "endemic", "epidemic" and "pandemic."

Which one is Antigenic Drift responsible for? Which one is Antigenic Shift responsible for?
Endemic- sporadic (localized to an area)

Epidemic- large number of people in an area are infected (Antigenic Drift)

Pandemic- large number of people across different areas affected (Antigenic Shift)
How do you distinguish between a Common Cold and the Flu?
Common cold= temp not high, headache is rare, no extreme exhaustion

Flu = high fever, headache, myalgia, malaise (not as much runny nose, sneezing, cough as the common cold)
What are the main medications to treat Influenza?
Amantidine and Rimantidine (inhibit M2 ion channel, not being used as much because of resistance)

Neuraminidase Inhibitors (zanamivir, oseltamivir)
What is the primary viral cause for Bronchiolitis?
RSV (respiratory syncytial virus)
On a pathophysiological level, what is causing wheezing and hypoxia (lack of oxygen) seen in Bronchiolitis?
RSV infect epithelial lining of bronchioles > necrosis > Edema, inflammation, increased mucus > closed airway causes air to get trapped and leads to HYPERINFLATED alveolar cells

*hypoxia due to lack of oxygen in blood even though there is still perfusion (because areas aren't ventilated)
How does the pathogenesis of RSV Bronchiolitis differ from RSV Pneumonia?
In RSV pneumonia, the cells lining alveolar spaces are infected, leading to necrosis and inflammation. Thus there is no exchange of oxygen and patient is unable to breathe.
T or F

The administration of Palivizumab, a prophylactic anti-RSV treatment, can help prevent the condition in high risk infants.
True

Typically for premature infants, or those with chronic lung disease or congenital heart disease.
Are ssRNA+ viruses genetically stable?
Yes!

They are non segmented (exception= arenaviridae, acquired from rodent)
What three major viruses are part of the Picornavirus family?
Rhinovirus
Enterovirus
Hepatovirus A (Hepatitis A)
What is the size of Picornaviruses?

What does a typical picovirviral particle contain?
Small!

Contains RNA genome + 4 structural proteins (VP1-VP4)
Coxsackievirus and most rhinoviruses bind to what receptor on cell surfaces?

What does Poliovirus bind to?
ICAM-1 (Intercellular Adhesion Molecule)

Another surface glycoprotein called CD155.
What is a canyon?
A structure on the virus's coat where host cell receptors bind.
What are the two molecules IRES and VPg responsible for in terms of viral replication?
RNA translation of picornaviruses

IRES= internal ribosome entry site (allows ribosomes to bind without a 5' cap)

VPg = primer for viral RNA-dependent RNA polymerase to bind (which makes complementary strand to -sense mRNA)
T or F

Even though the Enterovirus is a naked virus, it is capable of withstanding the GI tract?
True!

It can be transmitted via fecal-oral route and is stable at the low pH of the GI tract (excreted in stool)
What is the difference between Coxsackievirus A and B?
A= associated with 'Hand-food-and-mouth" disease (Herpangina, vesicular lesion)

B= associated with myocarditis and painful pleurodynia (Devil's grip)
Describe the life-cycle of the Poliovirus.
It can transmit via fecal-oral route (ingestion) > poliovirus enters via endocytosis > replicates in respiratory tract and intestinal mucosa and can spread to blood stream and thus establish viremia > shed in feces
T or F

Most Poliovirus infections will result in paralysis and damage of brain and spinal cord.
False

Almost 95% of cases are asymptomatc. Only 0.1-2% become paralytic.

Sometimes you get minor illness (fever, sore throat) and nonparalytic (flu-like symptoms, N/V/D that resolves) varieties
What specifically does Poliovirus target in the spinal cord and what symptoms does it produce?
It infects the anterior horn cells in the spinal cord resulting in paralysis and LMN signs (atrophy, decreased reflexes, paralysis)
What prophylactic options are there against Poliovirus?
1. Live attenuated vaccine (Sabin)- can establish mucosal immunity because poliovirus enters through intestinal mucosa

2. Killed (Salk) vaccine- humoral immunity
Is the Coronavirus:
enveloped or non enveloped
helical or icosahedral
RNA or DNA
cytoplasmic or nuclear replication
Corona virus=
Enveloped
Helical
RNA (largest +ssRNA virus)
cytoplasmic replication
Why is the Coronavirus, an enveloped virus, able to cause gastritis in infants?
Even though it has an envelope, it has a unique structure that is protective (glycoproteins are petal shaped and form "crown" around virus).
What novel corona virus caused a major worldwide outbreak in 2003?

Why does it make sense that a Coronavirus would undergo this scary transformation?
SARS (severe acute respiratory syndrome)

1. Coronaviruses are huge
2. They are RNA viruses, thus lack good proofreading from RNA polymerase
Why do Rhinoviruses (like coronavirus, a frequent cause of the common cold) not cause GI symptoms like Gastroenteritis?
Rhinoviruses like the temperature of Upper Respiratory Tract (cool). In addition, they infect nasopharyngeal epithelium preferentially. They do not establish viremia (spread).

*note Rhinoviruses are naked (even so, they don't survive in GI tract because of temperature)
What family of viruses is responsible for outbreaks of diarrhea and gastroenteritis (commonly on cruise ships)?

Name the prototypic virus of this family.
Caliciviruses

prototype= Norovirus or Norwalk virus
What are Reoviruses?
Respiratory Enteric Orphan

They are the only dsRNA virus with multiple segments. Most common cause of dehydrating diarrhea in kids.
What virus causes an estimated 25% of cases of Traveler's diarrhea?
Rotavirus (part of Reovirus family)

*mnemonic: Roto-rooter man (plumbing service, because inflicted individuals get diarrhea)
If the Reovirus is naked (non-enveloped), how does it survive the acids of the GI tract?
It has a double-layered coat (2 protein capsids). The outer layer is protective against the acidic environement of the GI tract.

This is also the only example we've learned of a virus that DIRECTLY PENETRATES cell.
T or F

People with the Rotovirus will commonly present with dysentery.
False!

Dysentery= mucous + blood in stools. This virus only lyses the epithelial cells on tip of vili and prevents absorption, causes fluid buildup leading to Diarrhea and malabsorption.

In other words, it is NONINVASIVE.
What are the most common types of viral hepatitis in the US?

What types cause acute infection?

What types cause chronic infection?
Hepatitis A,B, and C are most common in the US.

Type A and E cause acute, transient infection (spontaneously resolves).

Hepatitis B,C,and D may cause chronic infection (persistent viremia)
T or F

Symptoms of Hepatitis differ based on the type of virus (A-E)?
False

All the symptoms are the same:
Flu like, with N/V/D, Abdominal pain (RUQ), Fatigue, dark urine, clay colored stools, jaundice + icterus
What is the number one reason for liver transplant in the US?
Chronic HCV (Alcohol is the #2 reason)
Which viral hepatitis is associated with the most number of chronic infections worldwide?

Is the same one that is associated with the most number of chronic infections in the US?
Hep B

No. In the US it is Hep C (Hep B is prominent worldwide due to lack of vaccination in developing world)
What is the most common genotype of Hep C in the US?

How does genotype affect response to treatment?
Genotype 1

Genotype 2,3 more likely to respond to IFN-a treatment. Shorter course.

Genotype 1- longer course.
How is HCV transmitted?
Blood

-Injection drug use
- blood transfusion
- occupation needle stick
- PERMUCOSAL (Perinatal- through placenta, and sex involving blood)
T or F

Hep B is more infectious than Hep C or HIV
True

The chance of getting Hep B after exposure is 30% (Hep C is 3%, HIV is 0.3%)
T or F

A pregnant woman who has HCV should avoid breastfeeding her child to prevent transmission?
False!

HCV is transmitted through the blood. (note: most infants exposed to Hep C do well)
What country has the highest HCV prevalence?
Egypt

In hopes of treating schistosomiasis parasite, the CDC inadvertently infected whole generation via shared needles. This was in the 1950s before discovery of Hep C.
How do you diagnose HCV?

If a person affected by HCV has detectable RNA virus in their blood 5 months after the initial exposure, is their infection considered chronic?
Blood test (screen for antibody to HCV or viral genome)

No. For chronic infection, you must see viral RNA persistence for at least 6 months.
T or F

The Hep C virus is directly cytopathic.
False

It is not the HCV that causes damage to hepatocytes. Host immune response will cause collagen deposition (fibrosis) and lead to cirrhosis of liver.
Describe why the following symptoms occur with chronic HCV:

- Ascites
- Variceal bleeding
- Hepatic encephalopathy

Should you treat a patient who develops these symptoms?
Ascites- belly swelling due to albumin decrease, leaky fluid-- edema
Variceal bleeding- vein swell and can leak and pop
Encephalopathy- ammonia builds up, affects brain

Treatment will be ineffective because patient has decompensated. They will need liver transplant.
What does SVR (Sustained Virologic Response) refer to with respect to HCV?
The goal for drug therapy. It means that there is no detectable virus 6 months after stopping meds.

Hep C can be cured!
What is the main treatment for HCV?

Why do people hate this treatment so much?
Interferon-a. This is a natural immunomodulatory molecule that upregulates NK cells and lymphocytes to combat infection. It causes flu-like symptoms and has unpleasant non-specific side effects.
What is Pegylated Interferon?

Why is it better tolerated?
Attachment of non-toxic PEG molecule to Interferon

- gives drug longer half life (less injections)
- reduced clearance
- extends therapeutic action
What is Ribavirin and how does it work?
It is a pill that has been shown to enhance viral clearance with INF. It is a better option than INF along but not as good as Peg-INF
What are some common adverse effects of Pegylated Interferon?
Flu-like, fatigue
Blood marrow suppressant (anemia, neutropenia, decreased platelets)
Psychiatric (Depression, etc.)

Permanent effects:
- thyroid toxicity
- ophthalmologic toxicity
T or F

A person who has chronic hepatitis can look and feel completely normal.
True!

If this is the case, they should start on treatment because their liver has not decompensated to the point where all meds will be refractory.
What clinical tests will help you identify the extent of disease in a patient infected with HCV?
Bloodwork:
-Liver Enzyme tests: AST, ALT)
-Albumin (rarely done)
- Platelet count (if <160 it's problematic, means that spleen is swollen due to backed up blood)
- Bilirubin

Other:
- Fine needle biopsy
What are some new age medications for HCV?
DAAs = Direct Acting Agents
Drugs that DIRECTLY interfere with HCV replication by targeting specific enzymes.

Ex: Protease Inhibitors (PI)
- boceprevir
- telaprevir
Describe the structure of the Hepatitis B Virus.
Outer envelope with HBsAg (surface antigen)
Inner core Ag (HBcAg)
Inner polymerase that can reverse transcribe RNA --> DNA
small e antigen protein (HBeAg)
How does HBV replicate?
1. Entry into hepatocytes via HBsAg interaction.
2. After uncoating it is transported to nucleus where it forms cccDNA
3. Viral RNA is transcribed from cccDNA and sent to cytoplasm
4. In cytoplasm RNA is translated and packaged
5. reverse transcriptase is used to make DNA from RNA within particles
6. more proteins are packaged and finally when finished, baby virus is released
What is the one definite marker in the blood of a patient that could denote whether they have a chronic HBV infection?
Surface Antigen (HBsAg)

Everything else indicates an exposure to HBV (ex: antibody or even core antigen).
How is hepatocellular carcinoma in the setting of HBV different from hepatocellular carcinoma associated with HCV infection?
In HBV patients, they can sometimes go straight to carcinoma stage WITHOUT CIRRHOSIS first. (that's why it's very fatal and dangerous)
How is HBV transmitted?
Via contact with blood, semen, and other bodily fluids (exchanged during sex).

Also household close contact and Perinatal. Both horizontal and vertical transmission!
T or F

Presence of sAb in HBV infection indicates future recovery from infection and permanent immunity.
True

Once you have HBV surface antigen in your blood, it means that you have won! Thus a simple vaccine can truly save your life!
What is the mortality like if chronically infected with HBV?
1 out of 4 or 25% die :(
What are the two possible treatment options for patient infected with HBV?
1. Immunotherapy (INF- finite use)

2. Inhibitors of viral DNA polymerase (terminate new viral DNA strands)
What are some differences between use of INF for HBV and HCV?
HCV- it is the ONLY option (aside from now new Direct Acting Agents), also it can be curative!

HBV- not curative, there are other options that work better and have less side effects
With regards to HBV treatment, for oral agents, how long should the therapy last?
Once you start you have to continue. If you don't, you can develop resistance to medication.
What is the difference between HBV Vaccine and HBIG (immunoglobulin) and in what situations would you use each?
Vaccine= inactivated sAg, induces Ab and provides LONG TERM protection against HBV. 3 dose series (6 months total)

HBIG= concentrated Abs preparation from human plasma, provides temporary protection through passive transfer (ex: if a person is traveling to endemic area immediately)
If an HBV infected patient suddenly begins to deteriorate clinically, what differential diagnoses would you suspect?
1. HDV infection (enhances virulence)

2. Person is not compliant and stopped taking meds

3. Virus has somehow developed resistance
What Hepatitis virus is typically associated with outbreak infections?
Hepatitis A
What Hepatitis virus can be particularly life-threatening in pregnant women?
Hepatitis E
What Hepatitis virus is thought to perhaps be due to zoonotic infection and has increased incident in people who eat organ meats like liver and own pets?
Hepatitis E
What Hepatitis virus is solely dependent on another Hep virus to replicate?
Hepatitis D (Delta Virus)
What Hepatitis virus has an outer envelope with Small, Medium, and Large sAg proteins?
Hepatitis B
Retroviruses are:

- RNA or DNA
- ss or ds
- enveloped or non-enveloped
- icosahedral or helical
two copies of + ssRNA (DIPLOID!!)
enveloped
icosahedral
What is unusual about HIV in the context of other + sense RNA viruses?

What family does HIV come from?
It is the only one that cannot replicate immediately (because it doesn't have an RNA-dependent-RNA polymerase). To make RNA it has to first make DNA via a reverse transcriptase and then make RNA.

Lentivirus
Distinguish the shape of the HTLV (human t-lymphocytic virus) from HIV on an electron micrograph.
Retroviruses are classified based on capsid core (type B,C,D)

C-type (HTLV)- central core is icosahedral

D- type (HIV)- central core is cone shaped
What are the three major genes that all simple retroviruses carry?
1. gag = group specific antigen = Internal proteins (capsid, matrix, etc.)
2. pol = enzymes (reverse transcriptase, integrase, RNase H, protease)
3. env = envelope glycoproteins
What are the functions of the main enzymes in the HIV genome:

- Reverse transcriptase
- Integrase
- RNase H
- Protease
Reverse transcriptase: RNA --> DNA

Integrase: integrates viral genome into host genome
RNaseH (cleaves RNA as DNA is transcribed so complementary strand of DNA can be made)

Protease (cleaves proteins translated from mRNAs)
What does the "gag" genome or group-specific-antigen, code for?
Internal proteins (such as capsid, matrix, nucleic acid binding proteins)
What are the envelope proteins on HIV and what do they attach to on the host cell?

What is the role of a co-receptor?
Gp160 --> Gp120 + Gp41
Gp120- binds to CD4+ cell receptor
Gp41 initiates fusion of the host and virus membranes

Co-receptor (allow gp41 to fuse membranes)
CCR5- macrophages
CXCR4- helper T cells
What viruses are part of the Oncovirinae family and the Lentivirinae family?
Oncovirinae (carry oncogenes) ex: HTLV-1 and HTLV-2

Lentivirinae- HIV-1 and HIV-2

These are both complex retrovirus families
Describe the HIV lifecycle from entry to the formation of nascent viruses.
1. Entry via fusion of membranes
2. Release of genome into cytoplasm
3. Reverse transcriptase acts as an RNA-dependent-DNA polymerase to make DNA from RNA
4. RNA strand is degraded by RNase H
5. Reverse transcriptase acts as DNA dependent DNA polymerase and makes complementary DNA strand
6. dsDNA enters host cell nucleus and Integrase helps integrates into the host cell genome
7. New viral RNA is copied every time the cell copies it's genome.
8. Proteases help cleave new proteins and new virons assemble and are released from cell
What is a "provirus" in the context of retroviruses?

What is the role of LTR (long-terminal repeat) sequences that flank the genome?
Provirus= DNA intermediate (that integrates into the host genome)

These are non-coding, regulatory regions that help control gene expression (they contain enhancers and transcription factors)
Why are the Eastern Europeans somewhat resistant to HIV?
They don't express CCR5 (the co-receptor on Macrophages that assists in fusion of the membranes).
Why is it advantageous for HIV to target T cells?
Every time the host replicates, the viral genome will be replicated and new viruses can be made. The virus wants to integrate into a cell that proliferates often (ex: T cell which undergoes clonal proliferation)

Also, virus can be transmitted by T cell around body.
What types of cells does HIV infect?
1. CD4 T cells
2. Cells of Macrophage lineage (monocytes, macrophage, dendritic cells, microglia of brain)
What is a "flower cell"?
A helper T cell that has been infected with HTLV. Looks multilobulated (due to rapid cell proliferation)
What is the difference between the two types of Oncoviruses (Direct vs. Indirect)?
Direct (acute)= rapidly transform cells either by incorporating oncogene into viral genome or inserting activating factor/enhance existing genes. You typically tend to see this in a lab setting.

Indirect (transactivating)= promote uncontrolled cell growth, which can eventually lead to mutation and neoplasia.
What are oncogenes?
Proteins that are involved in growth control and differentiation.

ex: Growth factors, growth factor receptors, transcription factors, signal transduction proteins
What are some viruses associated with human cancers (name both the virus and the cancer)?
HPV --> genital tumors
EBV --> burkitt's lymphoma, nasopharyngeal carcinoma, b cell lymphoma
Hep B,C --> hepatocellular carcinoma
HTLV- ATLL (Adult tcell leukemia/lymphoma)
How can HTLV lead to ATLL (Adult T-cell leukemia/lymphoma)?
HTLV-1 infected Th cell forms syncytium with other cell > The "tax" transcriptional regulator causes cell to proliferate > eventually cell gains a mutation > this leads to development of ATLL
What HOST enzyme does the HIV virus use during it's process of replication?
RNA Polymerase II

After it integrates the provirus into the host genome, it acts like normal DNA transcription and translation.
T or F

The only way HIV can be spread is through an infected cell that travels around body.
False

There is a cell-free HIV that freely floats in plasma.
T or F

More than 10 billion virions of HIV are produced every day. An infected T cell will live for a maximum of 2 days after infection.
True

HIV is aggressive and rapidly replicates once it spreads to bone marrow and lymphoid tissue.
What does HIV become AIDS?
When infection has progressed to the point where people have severe infection.

1. CD4 count is less than 200 cells/mm^3

2. One or more of the terrible infections ex: strongyloidiasis, toxoplasmosis, pneumocystis penumonia, cryptococca meningitis, etc.
How does HIV affect the immune system (immune cells)?
- decreases CD4 Th cell function
- decrease NK cell activity (increase susceptibility to cancer)
- decreased ability for T cell to help B cells (can't produce antibody to new antigen)

Overall- Increased susceptibility to OPPORTUNISTIC INFECTION
Why might you see neurologic dysfunction and dementia in HIV infection (not related to specific condition like toxoplasmosis)?
Because HIV affects macrophage lineage cells including microglia in the brain.
T or F

HIV is highly contagious and thus a serious threat to medical workers.
False!

It is only transferred through intimate or body fluid innoculation. When working with needles use universal precautions (treat everyone the same).
What is the natural history of HIV (time course)?
1. Flulike (acute, mono-like illness)
2. Feeling fine (latent, virus replicates in lymph nodes)
3. Falling count (viral load increasing, T cell count decreasing)
4. Final crisis
What is a "set point" in terms of HIV?
A number that indicates how well a person's body can control viral load (lower set point = better control of viral load)

It is individualized for each person.
A patient comes in to your office. They have had a sexual encounter a few days ago with a male who they suspect is HIV+ and would like to be tested. You order an HIV antibody test that comes back negative for HIV. The patient is relieved that they are not infected. What do you tell them?
Unfortunately, in the situation of an early infection, antibody doesn't have time to develop. Need to wait and retest in 3 months. If clear then you can be sure.
What are two major groups of vector-borne pathogens?
Arthropod-borne (arbovirus)

Rodent-borne virus
T or F

In most cases, man is a dead-end host (i.e. infection of man is incidental and cannot be transmitted to another animal).
True

Exceptions: Dengue and Yellow fever
What is an Arbovirus?
It is an ARthropod-BOrne virus (hence "ar-bo")

replicates in arthropod vector (mosquito, fly, tick)
Most Arboviruses belong to what three virus families?

Are they RNA or DNA viruses?
-Togaviridae (alphaviridae)
- Flaviviridae
- Bunyaviridae

*ALL ARE RNA VIRUSES!
Distinguish between the Sylvatic and Urban cycles.
Sylvatic- transmission between arthropod and mammalian host ( and sometimes incidental transmission to man)

Urban- transmission between arthropod and man
What virus causes West Nile Encephalitis?

What is the natural reservoir for the virus and how is it transmitted?
West Nile = Flavivirus

Natural reservoir = birds
Transmitted by mosquito (Culex sp.)
A patient comes to you complaining of a fever for the past several days, a head, and a stiff neck. After several hours, they lapse into confusion and begin to convulse. Their relative says they had recently taken a hiking trip to the west coast and were bitten by several mosquitoes there. Based on the clinical symptoms, what virus might they be afflicted by?
West Nile

they are exhibiting signs of advanced disease- encephalitis. This can cause death if not properly treated.
What virus causes Dengue Fever?

What is the natural host and what is the vector (or the thing that transmits the virus)?
Flavivirus

Natural host= monkeys
Vector= mosquitos
Where in the world is Dengue fever most rampant?

What are some classic symptoms?
Tropics (Asia, Africa, Americas)

Sxs: fever, headache, rash, bone pain, myalgias, arthralgias. Sometimes called "BREAKBONE FEVER"
Describe the pathogenesis of Dengue Hemorrhagic Fever.
1st- dengue infects monocytes and causes mild, febrile illness.

2nd- subsequent infection with different serotype occurs. Abs produced from first attack bind to virus and ENHANCE infection.

*major problem= increased vascular permeability
Petichia- Subcutaneous hemorrhages- orbital hemorrhages
What serious complication can Dengue Hemorrhagic Fever lead to?
DSS or Dengue Shock Syndrome

(severe illness and shock due to vascular damage and loss of fluids)
What genera does the Hantavirus come from?

What is it's host and how is it transmitted?
Hanta from Bunyaviridae family

Rodent Host
Transmitted via aerosolization of rodent excretra (urine, dropping, etc)
What family do the Ebola and Marburg viruses come from?

What is their natural reservoir?
Filoviridae (Ebola)

Natural reservoir is UNKNOWN
What do the Ebola viruses look like on electron microscopy?
Pleomorphic (can take many forms) but typically funky, filamentous shape.
How can the Ebola virus be transmitted to humans?

What symptoms does it cause?
Transmission by infected monkeys/animals OR blood from patient.

Severe hemorrhagic fever, widespread bleeding (visceral organs and GI tract)
What family of viruses is made up of all rodent borne viruses?
Arenaviridae
T or F

The Togaviridae family contains only arboviruses (aka alphavirus)
False.

It also contains the Rubella virus (which causes German Measles). This isn't an arbovirus.
What are the two arbovirus-based diseases that we learned about in which man can continue the cycle of spreading instead of being a dead end host?

Why are these two the exception?
Yellow fever and Dengue fever

These are the only two viruses that establish high enough levels of blood viremia to allow the virus to be taken up by mosquitos.