Herpesvirus & Papillomavirus Flashcards

1
Q

what are some key characteristics of alphaherpesviruses?

A
  • variable host range
  • short reproduction cycle
  • rapid spread in culture
  • efficient destruction of infected cells
  • capacity to establish latency in sensory ganglia
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2
Q

HSV-1 infects where? HsV-2?

A

1: above the waist
2: below the waist

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3
Q

how is HSV-1 spread?

A

oral-oral or oral genital

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4
Q

how is HSV-2 spread?

A

primarily genital-genital, oral-genital also possible

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5
Q

where do alphaherpesviruses infect?

A

epithelial cells in the skin or mucosa; mucosa more susceptible

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6
Q

what is the incubation period for HSV-1/2?

A

2-14 days but typically 4-5

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7
Q

what are the symptoms of HSV1/2 infection?

A

flu-like, including localized lesions

only 1/3 show symptoms

lasts for 8 to 12 days

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8
Q

describe the latency assoc with HSV1/2

A
  • stationary cells, genome circularizes and stays as an episome in the nucleus
  • peripheral ganglia common site of latent infections
  • triggered by sunburn, systemic infection, immune impairment, stress
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9
Q

what is required for alphaherpesvirus to be overcome?

A

cell mediated immune response

  • people unable to produce antibodies can still handle herpesvirus infections
  • T lymphocytes detect antigens presented by MHC class I or II proteins
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10
Q

what does herpesvirus do to the immune response?

A

modulation of immune response

  • viral proteins bind antibodies and complement proteins
  • counter effects of interferon
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11
Q

how are alphaherpeviruses prevented?

A

avoid contact during active herpes recurrance

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12
Q

how are alphaherpesviruses treated?

A

acyclovir limits virus replication but will no eliminate latent infections

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13
Q

what are the key characteristics of betaherpesviruses?

A
  • restricted host range
  • long reproductive cycle
  • slow progression in cell culture
  • enlargement of infected cells (cytomeglia)
  • carrier cultures
  • latent infection in a variety of tissues
  • prototypical member: cytomegalovirus (CMV)
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14
Q

what are the key characteristics of gammaherpesviruses?

A
  • restricted host range
  • targets T & B lymphocytes
  • lytic infections
  • latency in lymphoid tissues
  • prototypical member: epstein barr virus (EBV)
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15
Q

what is Burkett’s lymphoma?

A
  • most common childhood cancer in equatorial Africa
  • tumor in jaw, eye socket, ovaries
  • in all cases, tumor cells have monoclonal EBV episome
  • role of EBV still not understood:
  • spur B cell growth, mutations or
  • genes transform cells
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16
Q

what is Hodgkin’s lymphoma?

A
  • 3 types:
  • NL:nodular sclerosing
  • MC:mixed cellularity
  • LD:lymphocytes depleted

** EBV present in 60-90% of MC & LD tumors, 20-40% of NL tumors

17
Q

what are the immune evasion antiviral host responses for beta/gammaherpesviruses?

A
  • intrinsic
  • innate
  • adaptive
18
Q

where does CMV persist?

A

in hematopoietic progenitor cells and macrophages in vitro

19
Q

is there latency with CMV?

A

no just chronic persistent infection

20
Q

how is CMV controlled?

A

by healthy, active immune system

21
Q

where does EBV persist?

A

in memory B cells

virus proteins ensure B cell proliferation and EBV genome replication

22
Q

how are beta/gammaherpesviruses treated and/or prevented?

A
  • infections are usually self limiting in immune competent individuals
  • antiviral therapy to inhibit viral genome replication, resistance can develop, and less effective at treating EBV
23
Q

what is the importance of immunoprophylaxis with CMV?

A

passive transfer of antibodies for prevention of CMV infection, transfer of EBV-specific T lymphocytes

24
Q

are there any vaccines for beta/gammaherpesviruses?

A

no

25
Q

what kind of virus is human papillmavirus?

A
  • papillomaviridae
  • genome: circular dsDNA
  • virion: non-enveloped
  • proteins:
  • L1-cell attachment
  • L2-membrane penetration
26
Q

T/F: plantars/palmars warts are human papillomavirus infections

A

T

27
Q

how does human papillomavirus enter the body and cell?

A
  • gain access thru abrasion of skin
  • est. infection in basal layer
  • cell pol required for genome replication
  • virus production in differentiating cells
  • non-lytic, virus released with dead cell shedding
28
Q

how is human papillomavirus infection acquired?

A
  • direct skin-to-skin contact, fomites
  • normal skin is very strong barrier
  • mucous membranes more susceptible
  • virus enters body thru abrasions
  • virus is hardy to environ. stresses; allows transmission via fomites
29
Q

what are the symptoms of human papillomavirus infection?

A
  • site of infection
  • take months to manifest
  • warts- raised or flat-~50% regress on their own in 2 years
30
Q

what is respiratory papillomatosis?

A

rare complication, respired virus, can be lethal

31
Q

how does oncogenesis - cervical cancer occur in human papillomavirus?

A
  • HPV requires actively replicating cells to replicate and produce progeny
  • E7 blocks retinoblastoma (Rb) protein- continued cell proliferation
  • E6 blocks the p53 suppressor pathway
  • actual path to cancer unknown: viral transformation, cell proliferation leading to cancerous mutation
32
Q

how is human papillomavirus treated and prevented?

A
  • most treatments ablative: liquid nitrogen, surgical excision, laser, caustic chemicals
  • no proof that condoms reduce risk
  • vaccination: Gardasil