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Virology 2 > Herpes > Flashcards

Herpes Flashcards

1
Q

describe the structure of a herpes virus

A

DNA, double strand, enveloped, icos

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2
Q

describe the herpes life cycle

A

adsorption and fusion w/ host

nucleocapsid releases viral DNA into nucleus

DNA becomes circular

mRNA, viral protein synthesis inside nucleus

progeny nucleocapsids assemble in nucleus causing inclusion bodies

viral glycoproteins are inserted into membrane (can cause syncitia)

progeny bud out from membrane

**needs nucleus

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3
Q

describe how herpes is eliminated from the body

A

herpes is not eliminated from the body, even upon asymptomatic recovery. instead, herpes becomes latent. even in asymptomatic latency, pts may sporadically create infectious virions

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4
Q

describe the subclassifications of herpes virus and some examples

A

alphaherpesvirus- HSV1- wide host range, latency in neurons

betaherpesvirus- CMV- narrow host range, latency in monocytes

gammaherpesvirus- EBV- narrow host range, latency in B lymphocytes

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5
Q

latency

A

all herpes viruses can become latent:

non destructive
lifelong
persistence of viral genome in non infectious state
potential to be reactivated

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6
Q

is latency active or static?

A

active-

creating gene products that prevent apoptosis, but opens the virus to immune recognition

also have asymptomatic shedding

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7
Q

why could herpes be good for you?

A

chronic stimulation of immunity by non-lethal pathogens could be beneficial

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8
Q

HSV1- primary and recurrent infection mechanisms

A

“cold sores”

primary infection often subclinical and most commonly causes stomatitis

virions produced at the site of initial infection travel up sensory neurons to nearest ganglion (often trigeminal ganglia) and establish latent infection

recurrent infection occurs when viral multiplication resumes and virions are tranported down axons to cutaneous site of primary infection- results in cold sores

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9
Q

what % of the population has HSV1?

A

> 80%

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10
Q

what is the incubation period for HSV 1

A

1-2 weeks

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11
Q

what factors can aggravate latency, causing a recurrent infection?

A

UV light
fever
emotion

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12
Q

HSV1 vaccine

A

none

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13
Q

HSV2

A

“genital herpes”

primary infection of genital mucosa, virus follows sensory neurons back to ganglia and establishes latency (sacral ganglia)

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14
Q

HSV2 incubation period

A

1-2 weeks

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15
Q

what % of the population has HSV2?

A

20%

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16
Q

describe the complications of HSV2 and perinatal infection

A

virions released by vaginal secretions can cause systemic disease in newborns ~6 days after birth

disease is often fatal, with destruction of liver and adrenal

most dangerous scenario is when mother has just gotten primary infection and has no Ab

HSV2 shedding before deliver is indication for C-section

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17
Q

HSV1 and 2 also cause what in addition to skin lesions

A

encephalitis

ocular disease

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18
Q

herpes simplex encephalitis

A

most common cause of sporadic encephalitis- usually HSV1

causes high fever, confusion, lymphocytes in CSF, lesions on MRI

often death w/o early recognition

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19
Q

treatment for herpes simplex encephalitis

A

acyclovir

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20
Q

herpes simplex keratitis

A

herpes simplex infection of eye

unilateral red eye

can cause blindness if untreated

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21
Q

does herpes simplex cross placenta

A

no

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22
Q

how do you diagnose herpes simplex?

A

isolation and culture
ELISA
DNA PCR of CSF
serology (IgM in primary infection)

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23
Q

HSV2 vaccine

A

none

24
Q

what are the treatments for herpes simplex

A

acyclovir- gold standard

herpes thymidine kinase will phosphorylate ACV, which can then be subsequently be phosphorylated by host and incorporated into DNA, which halts synthesis and causes death in infected cells

25
Q

varicella zoster virus

A

chickenpox/shingles

primary infection causes chickenpox- infection through respiratory tract- causes viremia. then spreads to the skin and
causes small itchy vesicles (rash) and fever. then travels retrograde to sensory neurons

often fatal to immunosuppressed

26
Q

varicella zoster virus transmission

A

aerosol

spread from mucosa in skin lesions to the respiratory tract. vesicles in respiratory tract may also rupture and spread disease

27
Q

treatment for varicella zoster virus

A

can get IgG- VZIG

or

acyclovir

28
Q

congenital varicella syndrome

A

fetal infection from a pregnant mother

causes limb atrophy and scarring of the skin

29
Q

zoster

A

shingles- more common w/ age

reactivation in a sensory ganglia that results in pain distributed along a specific dermatome, followed by lesions

can be followed by post-herpetic neuralgia- residual pain

more

30
Q

zoster treatment

A

acyclovir

31
Q

vaccinations to varicella zoster virus

A

vaccines to both varicella (live attenuated, requires boosting) and zoster

32
Q

CMV

A

causes enlarged cells w/ “owl eye” inclusion bodies

causes retinits, colitis, heterophile negative mono

leading cause of congenital abnormalities- from infection in 1st trimester- can go through placenta

33
Q

CMV immune evasion

A

has 6 genes to evade T cell activation via disrupting antigen presentation

34
Q

CMV transmission

A

blood/ bodily secretions (urine)

35
Q

CMV infects what

A

epithelia- moves to ganglia- infects monocytes

36
Q

easiest way to test for CMV in neonates

A

CMV in urine

37
Q

CMV vaccine

A

none

38
Q

CMV treatment

A

ganciclovir or foscarnet

39
Q

CMV findings in newborns

A 
retinal inflammation
jaundice
large spleen and liver
low weight
mineral deposits in brain
rash
seizures
small head
retardation
deafness
40
Q

EBV

A

causes heterophile positive mono and cancer

subclinical infections in kids, but more prevalent post puberty

1st symptom is sore throat
also: fever, sore throat, lethargy

41
Q

EBV transmission

A

salvia or oral contact

seen in college aged people

infects mucosal epithelia before spreading to B lymphocytes. can become latent w/ these b lymphocytes

seen in people post puberty

42
Q

EBV vaccine

A

none

43
Q

EBV incubation period

A

2-4 weeks

44
Q

% of population with EBV

A

90%

45
Q

describe the immune response to EBV

A

CTLs develop to clear infected B cells, causing abnormal cellular phenotype in blood

develop Abs that cross react w/ sheep RBCs, creating a diagnostic test

46
Q

diagnostic tests for EBV

A

look for CTLs or test for agglutination with sheep RBCs

Ig to viral capsid

47
Q

EBV treatment

A

no treatment

48
Q

HHV6

A

most prevalent herpes virus > 90%

genome can integrate w/ human genome and becomes heritable

causes: roseola infantum and exanthm subitum (rashes) w/ high fever

49
Q

HHV7

A

causes infections but w/o symptoms

50
Q

HHV8

A

Kaposis Herpesvirus

not seen in 1980s b/c of AIDS.
common in sexually transmitted HIV

forms spindle epidermal cells
also in GI and lungs

rarely seen in US b/c of antivirals

tumor virus

51
Q

HHV8 treatments or vaccines

A

none

52
Q

B virus

A

infection of rhesus macaques (benign in monkeys, not in humans)

very rare- seen in people who work in animal facilities

caueses encephalitis, serious neurological squelae, and death

53
Q

B virus treatment

A

acyclovir

54
Q

triflurodine

A

useful in treating keratitis simplex infections

causes nucleotide form of triflurodine to be incorporated into DNA and to halt DNA synthesis.

cells in cornea replicate slowly enough that only infected cells will die off

55
Q

adenine arabinoside

A

analogue of deoxyadenosine that gets phosphorylated by host enzymes an incorporated into DNA, halting DNA synthesis

56
Q

foscarnet

A

inhibits DNA polymerase of herpes virus selectively

alternative to ganciclovir in CMV

Virology 2 (6 decks)

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