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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

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
varicella zoster virus
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
varicella zoster virus transmission
aerosol spread from mucosa in skin lesions to the respiratory tract. vesicles in respiratory tract may also rupture and spread disease
27
treatment for varicella zoster virus
can get IgG- VZIG or acyclovir
28
congenital varicella syndrome
fetal infection from a pregnant mother causes limb atrophy and scarring of the skin
29
zoster
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
zoster treatment
acyclovir
31
vaccinations to varicella zoster virus
vaccines to both varicella (live attenuated, requires boosting) and zoster
32
CMV
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
CMV immune evasion
has 6 genes to evade T cell activation via disrupting antigen presentation
34
CMV transmission
blood/ bodily secretions (urine)
35
CMV infects what
epithelia- moves to ganglia- infects monocytes
36
easiest way to test for CMV in neonates
CMV in urine
37
CMV vaccine
none
38
CMV treatment
ganciclovir or foscarnet
39
CMV findings in newborns
``` retinal inflammation jaundice large spleen and liver low weight mineral deposits in brain rash seizures small head retardation deafness ```
40
EBV
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
EBV transmission
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
EBV vaccine
none
43
EBV incubation period
2-4 weeks
44
% of population with EBV
90%
45
describe the immune response to EBV
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
diagnostic tests for EBV
look for CTLs or test for agglutination with sheep RBCs Ig to viral capsid
47
EBV treatment
no treatment
48
HHV6
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
HHV7
causes infections but w/o symptoms
50
HHV8
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
HHV8 treatments or vaccines
none
52
B virus
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
B virus treatment
acyclovir
54
triflurodine
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
adenine arabinoside
analogue of deoxyadenosine that gets phosphorylated by host enzymes an incorporated into DNA, halting DNA synthesis
56
foscarnet
inhibits DNA polymerase of herpes virus selectively alternative to ganciclovir in CMV

Virology 2 (6 decks)

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