DNA viruses

Question 1

Common characteristics of DNA viruses

Answer 1

Transcription and replication occur in nucleus, use host RNA polymerase II to make mRNA, use either viral or host DNA polymerase for replication- smaller viruses use host

Question 2

What are the two ways that a DNA virus can get into the nucleus?

Answer 2

Direct passage through the nuclear pore or capsid docking on the nuclear membrane-depends on the size

Question 3

What steps are different between DNA viral replication and RNA viral replication?

Answer 3

RNA viruses use RDRP for mRNA synthesis and for genome replication
DNA viruses use host RNA polymerase for mRNA synthesis and can use either host or viral DNA polymerase for replication

Question 4

What do DNA viruses require in order to recruit RNA polymerase?

Answer 4

Promoter regions and virally encoded transcription factors (X,Y are host cell transcription factors that recognize the promoter on viruses)

Question 5

How are DNA polymerase and RDRP different?

Answer 5

DNA polymerase has a higher fidelity than RDRP; capable of proofreading so mutations are less likely and DNA viruses are more stable

Question 6

How is adenovirus classified?

Answer 6

dsDNA, linear, iscosahedral, naked

Question 7

What are the symptoms of adenovirus?

Answer 7

Respiratory: bad cold and fever, pharyngoconjunctival fever, laryngitis, pneumonia
Other: acute hemorrhagic cystitis, keratioconjunctivitis (eyes), gastroenteritis

Question 8

How is adenovirus transmitted?

Answer 8

Aerosol, fecal-oral, found in poorly chlorinated swimming pools

Question 9

Who are the susceptible populations for adenovirus?

Answer 9

Children (because no previous exposure) and military recruits at boot camp- there is a vaccine

Question 10

What is the life cycle for adenovirus?

Answer 10

1. Attachment via fiber protein 2. Endocytosis 3. Acidification causes partial uncoating 4. Directed to nucleus and enters through pore 5. Transcription 6. Translation - in phases (immediate early, early, late) 7. Replication using host DNA poly 8. Assembly in nucleus 9. Egress by lysis

Question 11

Who is generally treated for adenovirus? How are they treated?

Answer 11

Immunosuppresed; Cidofovir- still only used in dire cases

Question 12

How can adenovirus be diagnosed?

Answer 12

Culture, antigen detection, PCR, serology

Question 13

What diseases do human papilloma viruses cause?

Answer 13

Epithelial diseases: warts - common, plantar, genital

Malignancies: head and neck cancer, cervical cancer, penile cancer

Question 14

What tissue is HPV tropic towards?

Answer 14

Differentiated epithelial cells

Question 15

What is the life cycle for HPV?

Answer 15

Virus enters via cut/scratch, attaches and enters cells in epithelial basal lamina, when skin gets sloughed off virally infected cells move towards surface, when reaches the level of differentiation begins replication

Question 16

What is an episome? Which virus produces an episome?

Answer 16

Extracellular chromosome; HPV

Question 17

What does HPV use for DNA replication?

Answer 17

host DNA polymerase

Question 18

How is HPV diagnosis?

Answer 18

Serology- looking for antibodies to capsid (late gene product)

Question 19

How are warts treated?

Answer 19

Cryotherapy, chemical ablation (sialic acid), colopscopy- cryotherapy and chemical ablation just recruit the normal immune response

Question 20

What’s a VLP? Where is it used?

Answer 20

Viral Like Particles- an empty capsid used for vaccinations such as with gardasil and cervavix

Question 21

What types does Gardasil protect against? Cervavix?

Answer 21

Gardasil: 6, 11, 16, 18
Cervavix: 16, 18

Question 22

What is the host range for herpes viruses?

Answer 22

Only infect humans

Question 23

What DNA polymerase is used for herpes viruses?

Answer 23

Viral DNA polymerase

Question 24

Generally, what do immediate early, early, and late proteins encode?

Answer 24

Immediate early: transcription factors
Early: DNA polymerase
Late: capsid

Question 25

How does herpes virus get into the nucleus?

Answer 25

Fusion with the nuclear envelope- uncoats here

Question 26

Definition of Herpes virus latency

Answer 26

the genome is present in a cell but infectious virions are absent

Question 27

Why are vaccines difficult to make for herpes viruses?

Answer 27

Latency is established almost immediately, often before symptomatic; these genomes are maintained for the rest of the hosts life

Question 28

What cells do HSV, HCMV, and EBV infect?

Answer 28

HSV: neurons HCMV: hematopoetic stem cells in bone marrow EBV: B cells

Question 29

How is HSV-1 transmitted? What cells are infected? Where is latency established?

Answer 29

Transmission: Close contact with active lesion/asymp shedding, gingiostomatitis during childhood Infect: neurons Latency: trigeminal ganglia

Question 30

HSV-1 established in trigeminal ganglia is significant for what reason?

Answer 30

Access to the brain: meningitis in primary and can cause encephalitis in recurrent

Question 31

How is HSV-2 transmitted? Where are these lesions?

Answer 31

Spread by contact with mucus membranes (genital/oral), acquired in adult; lesions often below the waist

Question 32

How do you distinguish between HSV-1 and HSV-2?

Answer 32

HSV-1 above the waist lesions, transmitted by close contact, often acquired as baby HSV-1 below the waist lesions, transmitted by contact of mucus membranes, acquired as adult Differentiate by serology/PCR

Question 33

How are HSV-1/HSV-2 treated?

Answer 33

Can give antivirals (acyclovair) to shorten the infection and reduce transmission

Question 34

How is VZV transmitted? What are complications of VZV? Where is latency established?

Answer 34

Transmission: aerosol Complications: hepatitis, encephalitis, bacterial infection of lesions Latency: Dorsal root ganglia

Question 35

What disease occurs when get reactivation of latent VZV?

Answer 35

Herpes zoster (shingles)

Question 36

What are complications of Herpes zoster?

Answer 36

Bell's palsy, postherpatic neuralgia, retinitis

Question 37

How is VZV prevented? Treated?

Answer 37

Prevention: Vaccine available for both varicella and shingles (shingles is a booster but effective in decreasing postherpatic neuralgia) Treated: not required for uncomplicated VZV, only effective in first 3 days of outbreak for zoster

Question 38

How is EBV transmitted? What cells does it infect?

Answer 38

Transmission: saliva | Oral epithelial cells and B cells

Question 39

What is EBV recurrence linked to? What might recurrence cause?

Answer 39

Immunosuppression; malignancies (Hodgkins lymphoma, Burkitt's lymphoma, oral hairy leukoplasia)

Question 40

What does primary CMV infection look like?

Answer 40

Usually asymptomatic; when there are symptoms looks like mono except no sore throat and have a rash; may be jaundiced with hepatosplenomegaly

Question 41

Pregnant woman with a primary CMV infection- what are the risks for the fetus?

Answer 41

Vision loss, hearing loss, mental retardation, motor disabilities, seizures, death

Question 42

How is CMV treated?

Answer 42

Antivirals might be given like gancilcovir- but they are toxic and a suspected carincogen

Question 43

What cells does roseola infantum (HHV6 and HHV7) infect? How is roseola infantum transmitted?

Answer 43

CD4 T cells | Transmission: saliva

Question 44

What are the symptoms of HHV6/HHV7?

Answer 44

3 days of fever followed by a rash on trunk

Question 45

What types of hepatitis have a vaccine?

Answer 45

Hep A and B

Question 46

What things other than hepatitis can cause jaundice and need to be ruled out before diagnosis of hepatitis?

Answer 46

Reactions to prescription drugs, drug interactions, acetaminophen OD, ectasy

Question 47

How is Hep A classified?

Answer 47

human resistricted picornavirus, ssRNA, naked, icosahedral

Question 48

How is Hep A transmitted? Hep B? Hep C?

Answer 48

Hep A: fecal-oral Hep B: injection of infected blood, less frequently sex and birth Hep C: injection of infected blood, sex and birth

Question 49

What are symptoms of Hep A? How is it diagnosed? Treated?

Answer 49

Symptoms: usually asymp, but if symptomatic get gastroenteritis and acute hepatitis (due to immune response) Diagnosed: serology- look for antibodies to Hep A antigen (IgM/ IgG Treatment: 99% resolve without any intervention

Question 50

How is Hep B classified?

Answer 50

human restricted hepadnavirus, partially dsDNA, envelope

Question 51

What are the 4 stages in Hep B pathogenesis? What happens at each stage?

Answer 51

Immune tolerance (not recognized by immune), immunogenic symptoms (ALT levels increase), clearing symptoms (detection of Hep B antibody but no Hep B DNA), viral clearance

Question 52

What is the outcome for Hep B infection?

Answer 52

90% have acute hepatitis and then clearance 9% have Hep B antigens for more than 6 months and then progress to 4 different stages: resolution, asymptomatic carrier, chronic persistent, chronic active

Question 53

What is fulminant hepatitis?

Answer 53

Hepatic necrosis and encephalopathy; potentially fatal (seen in Hep A and B)

Question 54

How is chronic Hep B with liver damage treated?

Answer 54

polymerase inhibitors (reverse transcriptase inhibitor) and PEG-IFN for 6 months; transplant for late stage

Question 55

How is hep C classified?

Answer 55

flavivirus, (+)ssRNA, enveloped

Question 56

What is the outcome for HepC infection?

Answer 56

15% clear, 85% chronic leading to hepatocellular carinoma, cirrhosis, liver failure

Question 57

How is Hep c diagnosed?

Answer 57

Ezyme immunoassay for IgG followed by western blot (RIBA) for to avoid false positive

Question 58

How is Hep C treated during acute phase? Chronic?

Answer 58

Acute: may give PEG IFN Chronic: ribvarin + PEG IFN +HCV protease inhibitor