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IBI Test 1 > B3.012 Prework 1 VZV Biology and Pathogenesis > Flashcards

B3.012 Prework 1 VZV Biology and Pathogenesis Flashcards

1
Q

what is VZV?

A

varicella zoster virus

chickenpox

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2
Q

characterize the properties of VZV

A 
71 ORFs
lipid rich envelope into which viral glycoproteins are inserted
tegument layer
icosahedral nucleocapsid core
linear dsDNA genome
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3
Q

what is a tegument?

A

predominantly composed of viral regulatory proteins

matrix between nucleocapsid and envelope

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4
Q

describe the VZV cell cycle

A
  1. enveloped VZV particles attach to cell membranes, fuse and release tegument proteins
  2. capsids dock at nuclear pored where genomic DNA is injected into the nucleus and circularizes
  3. viral gene transcription and replication occur in the nucleus
  4. nucleocapsids are assembled and package newly synthesized genomic DNA
  5. capsids enter the cytoplasm and virion glycoproteins mature in the trans Golgi region and tegument proteins assemble in vesicles
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5
Q

what form of VZV can be transmitted?

A

aerosolized

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6
Q

what types of cells carry VZV to the resident T cells?

A

infected Langerhans cells
mucosal cells
plasmacytoid dendritic cells

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7
Q

where are resident T cells located?

A

draining lymph nodes

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8
Q

why do “chicken pox” develop on the skin?

A

infected T cells are induced to express skin homing factors
transport virus to dermal fibroblasts and keratinocytes
produce pro-inflammatory cytokines resulting in vesicles

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9
Q

what part of the sensory nervous system terminates in the skin?

A

afferent fibers

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10
Q

what components of the nervous system can varicella vesicles directly access?

A

dorsal root ganglia
cranial nerve ganglia
autonomic nervous system ganglia

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11
Q

what enables a second phase of replication to occur in skin?

A

reactivation from latency

causes lesion in the dermatome innervated by the affected sensory ganglion

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12
Q

where does VZV enter?

A

conjunctiva and upper respiratory tract

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13
Q

where does VZV replication occur?

A

regional lymph nodes

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14
Q

what is the mechanism behind viremia?

A

infected T cells

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15
Q

what follows the primary viremia of VZV?

A

replication in visceral organs

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16
Q

when does secondary viremia occur and what is the result?

A

14 days after contact

acute infection of skin and chicken pox rash

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17
Q

where is VZV latency established?

A

sensory ganglia of PNS

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18
Q

what is the reactivation of VZV called?

A

shingles

postherpetic neuralgia

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19
Q

what types of cells are affected following VZV incolulation/replication in respiratory cells?

A

tonsil T cells

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20
Q

how do T cells traffic into and out of tonsils?

A

through squamous epithelial cells that line tonsillar crypts

21
Q

why type of cells does VZV have an increased tropism for?

A

activated memory T cells that have skin homing markers

common in tonsils

22
Q

how are tonsil T cells with skin homing markers relevant in VZV?

A

programmed for immune surveillance
can transport the virus across capillary endothelial cells into skin
microvasculature extensive at base of hair follicles
initial VZV replication observed here

23
Q

retrograde transport

A

transport from the skin to the sensory neurons in the dorsal root ganglion and to the neurons of the enteric nervous system

24
Q

anterograde transport

A

following reactivation of VZV in sensory neurons
returns to skin and infects epidermis innervated by the infected neurons
reactivation of VZV within neurons of the ENS gives rise to local enteric disease

25
Q

what are 2 ways VZV can spread to dorsal root ganglia?

A
  1. T cell mediated spread directly to DRG

2. T cell mediated spread to skin and subsequent retrograde axonal transport to DRG

26
Q

what type of neuron cell bodies can VZV access?

A

nociceptive

mechanoreceptive

27
Q

what is the result of contiguous spread with viral transfer into new neuronal cell bodies?

A

amplifies opportunities for VZV delivery to skin sites of replication
over time, neuronal cell loss
indicated by satellite cell microproliferations

28
Q

nodules of Nageotte

A

satellite cell microproliferations

29
Q

what are potential complications associated with VZV?

A 
ophthalmic herpes zoster
delayed contralateral hemiparesis
Ramsay Hunt syndrome
encephalitis
myelitis
post herpetic neuralgia
30
Q

why might it be difficult to diagnose herpes zoster?

A

absence of rash
confusion w herpes simplex, impetigo, contact dermatitis, folliculitis, scabies…etc
children, young adults, and people with compromised immune systems more likely to have atypical presentations

31
Q

how can unequivocal confirmation of VZV diagnosis be obtained

A
  1. isolation of VZV in susceptible tissue culture cell lines
  2. seroconversion or a fourfold or greater rise in Ab titer between acute phase and convalescent phase
  3. detection of VZV DNA by PCR
32
Q

rapid impression VZV testing

A
  1. Tzanck smear
  2. PCR for detection of viral DNA in vesicular fluid
  3. immunofluorescent staining of cells from the lesion base or detection of viral antigens by assay
33
Q

most frequently employed serologic tools for assessing host response to VZV

A

immunofluorescent detection of antibodies to VZV membrane antigens aka fluorescent antibody to membrane antigen (FAMA)
immune adherence hemagglutinin
ELISA

34
Q

what is a Tzanck smear

A

scraping the base of the lesions in an attempt to demonstrate multinucleated giant cells
sens. 60%

35
Q

how does VZV differ from other herpes viruses?

A

assembled virions typically remain highly cell associated

fusion of infected and uninfected cells by viral glycoproteins produce multinucleated prokaryotes

36
Q

how does herpes simplex virus (HSV1-2) infect?

A

through mucosal membranes or breaks in the skin

37
Q

where does the HSV 1-2 virus replicate?

A

in the cells at the base of the lesion
infects the innervating neuron
travels by retrograde transport to ganglion

38
Q

epidemiology of HSV

A 
lifelong infection
recurrent diseases is source of contagion
asymptomatic shedding
transmitted orally, sexually, into eye, breaks in skin
HSV-1 = oral
HSV-2 = sexual
90% have antibody by age 2
HSV2 later in life w sex
39
Q

natural HSV disease manifestations in humans

A 
HSV encephalitis
cutaneous ulcers
genital ulcers
oral mucosa (herpes labialis)
corneal disease (keratitis)
40
Q

herpetic whitlow

A

infection of fingers by HSV

health care professionals at risk

41
Q

characterize EBV (HHV-4)

A

heterophile antibody positive infectious mononucleosis
associated w Burkitts lymphoma, Hodgkins disease, nasopharyngeal carcinoma, B-cell lymphomas in patients w immunodeficiency
hairy oral leukoplakia
mitogen for B cells immortalizes them

42
Q

briefly describe the EBV life cycle and pathogenesis

A

virus entry in buccal cavity
oropharyngeal mucosa infection
lymph node germinal center differentiation
peripheral circulation

43
Q

characterize CMV (HHV-5)

A

beta herpesvirus
dsDNA
largest virus to infect humans
not highly contagious
contracted from close personal contact with people who excrete the virus in body fluids
can also be shed from throat and uterine cervix

44
Q

CMV pathology

A

cell enlargement with intranuclear inclusions

cytomegalia in viscera and parotid glands

45
Q

immune suppressed end organ CMV diseases

A

encephalitis
retinitis
pneumonia
gastroenteritis

46
Q

diseases to which CMV is a contributing factor

A

glioblastoma

atherosclerosis

47
Q

consequences of congenital CMV passed to fetus through placenta

A

deafness

mental retardation

48
Q

characterize Roseola viruses (HHV 6-7)

A

spread via saliva
irritable, diarrhea, cough, fever for 3-7 days
as fever resolves faint macules develop on trunk and extremities that blanch upon pressure
rash resolves in 1-2 days

IBI Test 1 (15 decks)

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