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Supplemental Micro > DNA Viruses > Flashcards

DNA Viruses Flashcards

1
Q

where does DNA viral transcription and replication occur?

A

In the nucleus (except poxvirus)

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2
Q

what enzymes transcribe and replicate genome?

A

Host RNA polymerase (except poxvirus) and either viral or host DNA polymerase for replication

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3
Q

what dictates whether a virus uses viral or host DNA polymerase?

A

how large the virus is

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4
Q

what is the order of replication, transcription and translation in the DNA viral life cycle?

A

transcription, translation then replication

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5
Q

how is RNA polymerase recruited to transcribe viral DNA?

A

viral DNA has promotors that are regulated by both cellular and viral transcription factors (as long as the cell is permissive)

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6
Q

in what cellular condition is viral DNA polymerase needed?

A

when cells are differentiated and nondividing

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7
Q

what are two examples of viruses that use their own DNA polymerase?

A

herpesvirus and adenovirus

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8
Q

why do DNA viruses have less random mutation than RNA viruses?

A

DNA polymerases have higher fidelity and proof reading. They are genetically more stable

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9
Q

where is most genetic diversity created in DNA viral genomes?

A

in recombination within and beteen genomes

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10
Q

what types of diseases does adenovirus cause?

A

respiratory (cold, pharyngoconjunctival fever, pneumonia), acute hemorrhagic cystitis, keratoconjunctivitis and gastroenteritis

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11
Q

what is the transmission of adenovirus?

A

aerosol, fecal-oral, objects and poorly chlorinated swimming pools

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12
Q

what are two particular susceptible populations to adenovirus?

A

children and military recruits

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13
Q

what part of the virus facilitates adenovirus entry into the cell into the cytoplasm and how?

A

fibers (spikes) bind to cell receptors to cause endocytosis and acidification causes the spikes to lyse the vesicle

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14
Q

where and how does the capsid of adenovirus uncoat?

A

it uncoats at nuclear pore by injecting it through (capsid docks at pore)

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15
Q

what are the adenovirus gene expression phases?

A

immediate early (transcribing transcription factors), early (replication) and late (capsid proteins)

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16
Q

does adenovirus use host or viral DNA pol?

A

viral

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17
Q

where does adenovirus capsid assembly occur and how does it egress from the cell?

A

In the nucleus and it lyses out of the cell

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18
Q

how is adenovirus diagnosed?

A

cell culture, antigen detection, PCR and serology

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19
Q

when and how is adenovirus treated?

A

with immunocompromised patients in only most dire cases with cidofovir (nephrotoxic)

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20
Q

is there a vaccine for adenovirus?

A

yes but it is only available to military personnel

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21
Q

what is the most commonly diagnosed STD in the US?

A

HPV

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22
Q

what epithelial diseases and malignancies are caused by HPV?

A

common warts, plantar warts and genital warts. head, neck, cervical and penile cancer

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23
Q

what is the tropism of HPV?

A

differentiated epithelial cells

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24
Q

what is the mechanism of wart formation associated with HPV?

A

HPV infects the precursor skin cells (stratum corneum) with little amplification. Once cells differentiate and become keratinized, the virus begins to replicate and cause hyperplasia

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25
Q

why is it difficult to study HPV in culture?

A

transcription factors in late keratinocytes promote gene transcription

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26
Q

what are the two possible courses of disease for a HPV wart?

A

it can be resolved by the host’s immune system or it may transform into a tumor from viral transcription factors E6 and E7 (oncogenes)

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27
Q

does HPV use host or viral polymerase?

A

Host

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28
Q

why is it important to diagnose ant type genital HPV?

A

there are 13 high risk types of cancer causing HPV (type with DNA tests)

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29
Q

how are HPV warts and malignancies treated?

A

cryotherapy, chemical ablation and colposcopy (excision in the cervix). ANy malignancies should be treated with oncotherapy

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30
Q

what are the types of vaccines for HPV and what types are they active against?

A

gardasil: 6,11,16 and 18
cervarix: 16 and 18

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31
Q

what is the vaccine to HPV comprised of?

A

VLPs: virus-like particles (empty capsids)

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32
Q

how many speicies of herpesviruses are there and what is the average number that people are infected with?

A

8 and most people are infected with >3

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33
Q

how long does a herpesvirus take to clear up?

A

it doesn’t

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34
Q

what is the host range and tropism of herpesvirus?

A

only infectious in humans and each virus prefers different cell types

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35
Q

where does herpesvirus transcription take place?

A

in the host cell nucleus

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36
Q

what phases of expression do herpesviruses have?

A

immediate early (transcription factors), early (replication of genome) and late (capsid proteins)

37
Q

how does herpesvirus replicate its DNA?

A

viral polymerase and accessory factors

38
Q

how does herpesvirus egress?

A

exocytosis

39
Q

what is the definition of herpesvirus latency?

A

genome is present in cell but infectious virions are absent

40
Q

what is a major barrier to vaccines with herpesviruses?

A

latency of the virus is established before it could be identified by the immune system and stays there for life

41
Q

herpesvirus is only contagious during active disease periods. True or false?

A

false. they are transmissable during periods of latency as well (asymptomatic shedding)

42
Q

how often do latent herpesviruses recur?

A

they may reoccur never or often

43
Q

how is HSV-1 transmitted?

A

close contact with active lesions or asymptomatic shedding

44
Q

what is the primary disease of HSV1 in childhood?

A

gingivostomatitis

45
Q

where are the primary lesions of HSV1 usually present and where is latency established?

A

above the waist (can be genital) and neurons

46
Q

what triggers and precedes recurrence of HSV1?

A

triggered by fever, sunlight or stress (etc) and it is preceded by a tingling, itching prodrome

47
Q

where are the lesions of HSV1 recurrence?

A

on lips or in mouth (may also be in eyes, on genitals or on fingers)

48
Q

what is often a complication of primary infection with HSV1 and 2?

A

meningitis (stiff neck and headache)

could also cause encephalitis

49
Q

what part of the brain is targeted by HSV1?

A

the temporal lobe

50
Q

how is HSV2 disease spread?

A

by close contact between mucous membranes (usually acquired during adulthood)

51
Q

what are the symptoms of primary HSV2 disease?

A

many lesions, pain, itching, fever and headache (not always but usually below the waist)

52
Q

where is latency established?

A

in neurons

53
Q

double infections with HSV1 and 2 are uncommon. True or False?

A

False. They are actually common

54
Q

what are the symptoms of recurrent HSV 2 disease?

A

prodoromic itching and tingling followed by vesicular lesions on labia, penis, anus, mouth etc.

55
Q

how is HSV diagnosed?

A

serology and PCR disinguish HSV 1 and 2 (differentiates risk for having children)

56
Q

when are antivirals used for HSV?

A

to shorten an infection, reduce transmission and as prophylaxis when people have frequent outbreaks

57
Q

what is the main antiviral used for HSV?

A

acyclovir

58
Q

how is HSV prevented?

A

safe sex, avoidance of cold sores, and chemoprophylaxis to reduce shedding

59
Q

are there any vaccines for HSV?

A

no

60
Q

what is the primary infection of VZV?

A

chicken pox- “dew drops on rose petals” rash

61
Q

how is Varicella transmitted?

A

aerosol (highly contagious)

62
Q

what are some complications of VZV primary infection

A

hepatitis, encephalitis, pneumonitis or bacterial infection of lesions

63
Q

what is recurrence of VZV and what latency is it caused by?

A

shingles (herpes zoster). caused by a latency in dorsal root ganglia

64
Q

who is most likely to develop shingles?

A

elderly and immunocompromised carriers of VZV

65
Q

where does outbreak of shingles occur?

A

along the skin surface of a single dermatome

66
Q

what are some complications of shingles?

A

bell’s palsy, posterpetic neuralgia (indefinite pain) and retinitis (can cause infectious blindness)

67
Q

what is shingles infection of the eye called?

A

Herpes Zoster Opthalmicus

68
Q

what parts of the eye can be effected by zoster and what part can be destroyed?

A

all parts can be infected and it can destroy the retina

69
Q

how is VZV diagnosed?

A

clinical signs, PCR, antigen and serology

70
Q

how and when is VZV treated?

A

not required unless complicated. can be treated within 3 days of beginning of zoster symptoms to have relief. Treat with acyclovir and foscarnet (second line)

71
Q

how is VZV prevented?

A

two live, attenuated vaccines:
varvax prevents varicella (1-50)
zostavax prevents zoster (>50 yo)

72
Q

how is Epstein Barr Virus transmitted and what cells does it infect and become latent in?

A

it is transmitted in saliva and infects oral epithelial cells and B cells in tonsils. It remains latent in B cells

73
Q

what are the usual symptoms of childhood Epstein Barr Viruses?

A

they are usually asymptomatic

74
Q

when is EBV likely to recur?

A

during ties of imunosuppression (usually does not occur in healthy people)

75
Q

what complications are associated with latent EBV virus?

A

many different types of malignancies and oral hairy leukoplakia

76
Q

how is infectious EBV diagnosed?

A

clinical signs, serology and blood smear for elevated WBC and atypical lymphocytes

77
Q

how are EBV associated malignancies treated?

A

alleviate symptoms, treat immunosupression and treat with oncotherapy

78
Q

what antivirals and vaccines are available for EBV?

A

none

79
Q

how does CMV spread and what are its symptoms?

A

many different routs. symptoms may like mono but are highly dependent upon the host (most people are asymptomatic)

80
Q

how can CMV and EBV be differentiated clinically?

A

CMV has no sore throat but does have a rash

81
Q

what is the result of primary infection with CMV in pregnancy?

A

increased risk of congenital malformations. primary cause of deafness

82
Q

in which patients is CMV concerning?

A

pregnant women, AIDS patients and transplant recipients (frequent cause of transplant failure)

83
Q

how is CMV diagnosed?

A

serology, culture and PCR

84
Q

what antiviral drugs are used for CMV?

A

ganciclovir, foscarnet and cidofovir (last two nephrotoxic)

85
Q

what disease is caused by HHV6b and HHV7 and how is it transmitted?

A

roseola infantum, transmitted orally

86
Q

what are the symptoms of roseola and what age does it typically happen?

A

3 day high fever followed by faint rash. happens most at 7-13 months of age

87
Q

how is roseola treated?

A

supportive care for fever but resist giving antibiotics

88
Q

what must be ruled out when diagnising roseola infection?

A

drug allergy

Supplemental Micro (8 decks)

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