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Viruses, fungi, parasites > DNA viruses > Flashcards

DNA viruses Flashcards

1
Q

Common characteristics of DNA viruses

A

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

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2
Q

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

A

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

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3
Q

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

A

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

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4
Q

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

A

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

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5
Q

How are DNA polymerase and RDRP different?

A

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

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6
Q

How is adenovirus classified?

A

dsDNA, linear, iscosahedral, naked

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7
Q

What are the symptoms of adenovirus?

A

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

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8
Q

How is adenovirus transmitted?

A

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

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9
Q

Who are the susceptible populations for adenovirus?

A

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

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10
Q

What is the life cycle for adenovirus?

A
  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
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11
Q

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

A

Immunosuppresed; Cidofovir- still only used in dire cases

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12
Q

How can adenovirus be diagnosed?

A

Culture, antigen detection, PCR, serology

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13
Q

What diseases do human papilloma viruses cause?

A

Epithelial diseases: warts - common, plantar, genital

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

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14
Q

What tissue is HPV tropic towards?

A

Differentiated epithelial cells

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15
Q

What is the life cycle for HPV?

A

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

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16
Q

What is an episome? Which virus produces an episome?

A

Extracellular chromosome; HPV

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17
Q

What does HPV use for DNA replication?

A

host DNA polymerase

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18
Q

How is HPV diagnosis?

A

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

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19
Q

How are warts treated?

A

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

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20
Q

What’s a VLP? Where is it used?

A

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

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21
Q

What types does Gardasil protect against? Cervavix?

A

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

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22
Q

What is the host range for herpes viruses?

A

Only infect humans

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23
Q

What DNA polymerase is used for herpes viruses?

A

Viral DNA polymerase

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24
Q

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

A

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

25
Q

How does herpes virus get into the nucleus?

A

Fusion with the nuclear envelope- uncoats here

26
Q

Definition of Herpes virus latency

A

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

27
Q

Why are vaccines difficult to make for herpes viruses?

A

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

28
Q

What cells do HSV, HCMV, and EBV infect?

A

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

29
Q

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

A

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

30
Q

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

A

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

31
Q

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

A

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

32
Q

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

A

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

33
Q

How are HSV-1/HSV-2 treated?

A

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

34
Q

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

A

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

35
Q

What disease occurs when get reactivation of latent VZV?

A

Herpes zoster (shingles)

36
Q

What are complications of Herpes zoster?

A

Bell’s palsy, postherpatic neuralgia, retinitis

37
Q

How is VZV prevented? Treated?

A

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

38
Q

How is EBV transmitted? What cells does it infect?

A

Transmission: saliva

Oral epithelial cells and B cells

39
Q

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

A

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

40
Q

What does primary CMV infection look like?

A

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

41
Q

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

A

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

42
Q

How is CMV treated?

A

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

43
Q

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

A

CD4 T cells

Transmission: saliva

44
Q

What are the symptoms of HHV6/HHV7?

A

3 days of fever followed by a rash on trunk

45
Q

What types of hepatitis have a vaccine?

A

Hep A and B

46
Q

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

A

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

47
Q

How is Hep A classified?

A

human resistricted picornavirus, ssRNA, naked, icosahedral

48
Q

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

A

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

49
Q

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

A

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

50
Q

How is Hep B classified?

A

human restricted hepadnavirus, partially dsDNA, envelope

51
Q

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

A

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

52
Q

What is the outcome for Hep B infection?

A

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

53
Q

What is fulminant hepatitis?

A

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

54
Q

How is chronic Hep B with liver damage treated?

A

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

55
Q

How is hep C classified?

A

flavivirus, (+)ssRNA, enveloped

56
Q

What is the outcome for HepC infection?

A

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

57
Q

How is Hep c diagnosed?

A

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

58
Q

How is Hep C treated during acute phase? Chronic?

A

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

Viruses, fungi, parasites (5 decks)

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