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38 Cards in this Set

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  • Back
1. ds DNA
2. linear
3. Naked
4. Ocosahedral
5. Respiratory, Conjunctivitis, ARD
1. ss linear DNA
2. Naked
3. Ocosahedral
4. B19: erythema infectiosum (5th disease) Slapped check appearance. Trans: respiratory.
In adults: polyarthritis.
Fetus: life-threatening anemia, CHF.
1. ds circular DNA
2. Naked
3. Icosahedral
4. 3 diseases:
a. HPV - skin,genital, larngeal warts, cervical ca.
b. BKV - assoc c kidney transplant.
c. JCV - progressive multifocal leukoencephalopathy.
(later 2 cause mild respiratory infection, then establish latency in 80%.
1. ds DNA.
2. VERY complex structure
3. Enveloped, but STABLE
4. Replicates in CYTOPLASM
5. 50% mortality = variola major
1% mortality = variola minor.
6. No animal reservoir.
7. Trans: hu-hu via respiratory or skin lesions.
8. 2 week incubation.
Differentiate between alpha, beta and gamma subfamilies of herpes.
alpha: variable host range, rapid reproductive cycle, latency in neurons.

beta: restricted host range, slow reproductive cycle, latency in lymphocytes & monocytes, cytomegalic.

gamma: restricted host range, latency in lymphoid cells, lymphotropic.
General features of herpes viruses.
1. DS linear DNA.
2. Enveloped.
3. Have spikes for penetration (glycoproteins).
4. Icosohedral.
5. Tegument (e- dense material b/w capsid & envelope; contains proteins that can be released ready to act.
3 common features of productive herpes infections.
1. cytolytic
2. viral DNA synthesis in nucleus, carried out by virus-encoded enzymes.
3. Nucleocapside assembled in nucleus & gains envelope.
List the 8 types of herpes virus.
1. HSV-1
2. HSV-2
3. Varicella-Zoster
4. EBV
5. Cytomegalovirus
6. Herpes virus 6
7. no human diseases.
8. Herpes virus 8
2 requirements for persistent herpes virus to be established.
1. Suppress cytolytic activites.
2. Avoid host antiviral defenses.
Which herpes viruses are subfamily alpha?
1. HSV-1
2. HSV-2
3. Varicella Zoster
Which herpes viruses are subfamily beta?
1. Cytomegalovirus
2. HHV-6
3. HHV-7
Which herpes viruses are subfamily gamma?
1. EBV
2. HHV-8
Char. of HSV-1
1. oral & ocular infections.
2. Primary infection usually asymptomatic in early childhood. Symptomatic in children: sore throat, fever, cervial lymphadeopathy, gingivostoatis. IN adults: pharyngitis, tonsillitis, lymphadenopathy.
3. Keratoconjuncitivitis (principal infectious cause of blindness in developed world).
4. Latency in neurons.
5. Latency-associated transcripts (LAT) - facilitate latency.
6. Low neuroinvasivenss; high neurovirulence.
7. Most common cause of viral encephalitis.
Char. of HSV-2
1. genital infection.
2. Symptom: vesicular, ulcerative lesion, fever, malaise, dysuria.
3. HSV genital ulcers increase rate of HIV infection.
What is recurrent herpetic stromal keratitis?
An autoinflmmatory reaction that is T-cell dependent.
3 possible mechanisms:
1. Molecular mimicry
2. Bystander activation (T cells respond to antigen X and end up responding to antigen Y).
3. Inflmmatory cells release cytokines, disrupting angiogenic vs. anti-angiogenic balance.
How is HSV reactivated from latency? 2 steps.
1. Viral Fc-gamma receptor inhibits Ab-dependent cell-mediated cytotoxicity. (blocking effector function)
2. Viral complement receptor binds C3b and prevents binding of properdin and C5. (prevents complement activation)
3. Evasion ofCD8+ T cells by inhibitory TAP which is needed for MHC-I presentation.
What is the mechanism of action of acyclovir against HSV1 and 2?
Guanosine analogue. Triphosphorylated form is incorporated into gorwing DNA chain, resulting in premature termination.
What are the products of
1. alpha
2. beta
3. gamma
herpes genes?
1. alpha: transcriptional regulatory proteins & ICP47 (inhibits TAP).
2. Beta: minor structural proteins and proteins required for viral DNA synethesis.
3. gamma: major structural proteins.
What is bystander activation?
Method of reactivating HSV1 or 2. Involves release of antigen from host cell that transforms host cell protein structure into an immunogenic protein.
Char. of Varicella-Zoster.
1. Chickenpox (varicella); shingles (reactivated).
2. Spread via respiratory secetions.
3. Zoster (shingles)produces unilateral rash, preceeded by severe pain. complication: postherpetic neuralgia.
Name 6 complications of VZV infections.
1. Secondary bacterial skin infections.
2. VZV pneumonia (10-40% mortality in adults)
3. VZV encephalitis
4. VZV hepatitis
5. Reye's syndrome
6. During pregnancy, congenital varicella syndrome of fetus.
What is congenital varicella syndrome?
Complication of VZV that occurs during pregnancy. 1-41% mortality rate. Caues skin lesions, neurologic/skeletal defects. 30% of infected infants die within several months of birth.
Vaccine for varicella?
Attenuated (Oka VZV vaccine). can sometimes establish latent infection & reactivate later to cause zoster.
Treatment for varicella?
1. Postexposure vaccine w/i 3 days of exposure.
2. Passive immunization.
3. Acyclovir (IMC).
Char. of Epstein-Barr.
1. gamma subfamily.
2. B-lymphotropic.
3. Causes lifelong persistent infection.
4. Symptoms: children - asymptomatic; adolescents - infectious mono
5. Also causes X-linked fatal infectious mono, oral hairy leukoplakia (AIDs), numerous cancers.
Epstein-Barr-associated malignancies.
1. Endemic Burkitt's lymphoma.(cancer of childhood)
2. Immunoblastic B-cell lymphoma/post-transplant lymphoproliferative disease.
3. Undifferentiated nasopharyngeal carcinoma.
5 lines of evidence for causal role of EBV in development of Burkitt's Lymphoma (a B cell lymphoma of childen).
1. Close Association.
2. Monoclonality of tumors. (
3. Ability of EBV to drive prolieration of B cells in culture.
4. Seroepidemiology.
5. Ability of EBV to drive proliferation of B cells in vivo
What is immunoblastic B-cell lymphoma?
occurs in IMC, & transplant pts.
Char of Human Cytomegalovirus.
1. Ubiquitious in body fluids.
2. Primary site of infection in epithelial cells..
3. Latency in monocytes.
4. Beta subfamily.
5. cytomegalic inclusion disease in fetus and neonate.
6. IMC: pneumonia, hepatitis, intractable diarrhea, retinitis.
7. no vaccine.
8. Constantly evades the immune system.
Char of Herpes virus 6.
1. Usually acquired in infancy/early childhood.
2. Causes Roseola (exanthem subitum).
3. Trans: saliva.
4. Beta subfamily.
5. Latency: T cells, macrophages.
Char of Herpes virus 8.
1.beta subfamily.
2. Present in most/all Kaposi's sarcoma, a vascular tumor composed of spindle cells, inflammatory cells, extravasated erythorcytes.
2. HV8 carries may genes it has stolen from the huan genome.
Char of Papilloma Virus.
ds DNA, circular genome.
Protein coat with 2 capsid proteins.
Are early and late (structural) proteins.
E2 (transcription factor) and E1 (replication factor).
Enter via break in skin/mucous membrane..moves to basal cells..limited replication..latent shage...early viral (RNA), then late viral stage (RNA,DNA)..virus shed in superficial layer. (spreads from horizontally & vertically).
Causes:1. skin warts. 2. geneital warts. 3. respiratory papillomas.
What 2 genetic changes are associated with papilloma transformation into carcinoma.
1. E6 and E7 are ALWAYS maintained.(E7 binds RB/turns off.E6 targets p53 for degradation).
2. E2 is lost.(negative reg. of E6 and E7).
Which papilloma viruses are associated mostly strongly with cervical cancer?
HPV 16 and HPV 18
What are the capsid proteins of papilloma virus?
L1 (major) and L2 (minor)
Association b/w papillomas and COX-2.
overexpress COX-2 and have high PGE2 levels (prostalgandins).
Papilloma-induced diseases.
1. Skin warts.
2. Skin cancers in Epidermodysplasia verruciformis
3. Respiratory papillomas
4. Genital infections.
Lower risk HPV viruses for cervical cancer.
HPV6 & 11.