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PATH310 > HPV 2 > Flashcards

HPV 2 Flashcards

1
Q

higher incidence cervical cancers in? rare in?

A

married women, widows, prostitutes. virgins, nuns.

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2
Q

hpv16, 18 isolated from

A

cerv cancer biopsies, cloned in 1983/4

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3
Q

papillomaviruses

A

small, non-enveloped, circular dsDNA genome

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4
Q

HPVs are species specific & widespread among what

A

mammals

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5
Q

how many types HPVs ID’d? sequenced? exist ?

A

100 ID’d, 80 seq’d, 200 exist based on partial seq frags

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6
Q

is HPV serological prevalence ubiquitous in pop?

A

yes, most common STI globally

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7
Q

global HPV prevalence

A

normal cytology reports, MA-compiled data, some studies used PCR, others used serology.

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8
Q

highest & lowest HPV prevalence

A

africa highest, europe lowest. (US numbers suggest prevalence rates higher)

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9
Q

cervical cancer freq

A

2nd most freq cancer in women

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10
Q

HPV causes ? cases of cerv cancer

A

all cases of cerv cancer. approx 4% all cancers

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11
Q

HPV also responsible for proportion of VVAP cancers

A

vaginal, vulvar, anal, penile cancers

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12
Q

cerv cancer rates 10x higher in areas w/o

A

w/o cytology screening

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13
Q

screening programs good at detecting most cerv cancers (aka?) but not good at detecting ?

A

(aka squamous cell carcinomas) but hard to detect adenocarcinomas

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14
Q

HPV exposure

A

~high. 75% pop at some point

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15
Q

incubation period HPV

A

unclear. 3 months - several yrs

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16
Q

HPV infection in US

A

60% have presence of Abs (neg HPV test), 10% HPV dna pos but colposcopy neg, 4% colposcopy pos (1% get gential warts, less get cancers)

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17
Q

most HPV transmissions occur

A

from sex/ skin-skin contact w infected person

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18
Q

is insertive/receptive sex necessary

A

no. contact w mucous memb is enough

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19
Q

condoms decr transmission but

A

dont protect completely

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20
Q

risk of fomites mediated transmission

A

not clear but probable. (share inanimate objects)

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21
Q

HPV transmission for M/F

A

M - penile cancer
F - cervical cancer
both - genital warts, anal cancer, etc

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22
Q

incr risk of cervical cancer w ?

A

sex, age, age of 1st sex, co-infections, M circumcision, condom use, lifetime # partners

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23
Q

HPV prevalence incr when?

A

around age of onset of sex. decline w age!

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24
Q

dramatic incr in cerv cancer cases bw what age

A

20 - 45

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25
Q

incr risk of HPV prevalence w what

A

other STIs (like HIV)

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26
Q

HPV types 16, 18 (high risk, lead to pre/cancerous lesions)

A

cause 70% cerv cancer cases (squamous cell)

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27
Q

HPV 6, 11 types (low risk, lead to condylomata acuminata)

A

cause 90% genital warts cases

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28
Q

HPV infection clin manifestations

A

cutaneous , anogenital warts. epidermadysplasia verruciformis. resp papillomatosis. other HPV infections

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29
Q

cutaneous warts

A

~asymptomatic, 50% resolve within 1 yr, rare but can degrade into carcinomas

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30
Q

anogenital warts

A

past history of anal warts, incr anal cancer 10x risk. vulvar condylomata acuminata

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31
Q

epidermadysplasia verruciformis

A

autosomal recessive genodermatosis linked to gene in xsome 17. appear in 1st decade of life, transformto invasive squamous carcinoma (malig)

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32
Q

respiratory papillomatosis

A

hoarseness. altered cry & resp fail, often for infants. obstruct trachea, lungs. require excision

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33
Q

other HPV infections

A

most common = oral squamous pappillomas. involve diff mucus membs (eyes, mouth)

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34
Q

HPV genome how many bps? ORFs which encode what proteins?

A

7900 bps, 8 ORFs - encode 6 early proteins, 2 late structural ones.

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35
Q

viral gene exp linked to differentiation state of infected epithel

A

suprabasal epithel cells - early gene exp. terminally differentiated karatinocytes - late gene exp.

36
Q

HPV disease mech (aidasi)

A
  1. micro abrasion in mucosa
  2. infect basal keratinocytes
  3. differentiate, move to distal mucosa
  4. viral assembly as cells move to mucosa
  5. infectious virus shed
  6. xsomal integration
37
Q

most infections result in

A

viral clearance (mechs unclear), develop type-specific immune response

38
Q

development of invasive cancer closely linked to

A

viral DNA integration

39
Q

integration of viral dna leads to

A

overexpress E6, E7 to target p53, pRB. which incr cell prolif, decr repair > mutations > CIN > invasive cervical cancer

40
Q

in basal cells, HPV viral dna replic occurs where, in what fashion, at what rate?

A

in squamous epithel cells. episomal fashion. low rate. 50-100 copies/cell

41
Q

infected basal cells enter what

A

suprabasal cell layer, assoc w incr exp of early, late proteins E4 5 6 7

42
Q

viral assembly occurs in what cells

A

terminally differentiated epithel cells (exp of L1, L2 proteins)

43
Q

what occurs after viral assembly

A

virions released into tissue, infection spreads

44
Q

viral integration takes place where?

A

in small proportion of basal lamina cells

45
Q

viral integration is important for?

A

develop malignant disease (but not sufficient)

46
Q

integration of HPV genome into xsome leads to

A

uncontrollable oncoprotein prod, host cell transform

47
Q

other mechs playing key role in cancer develop incl.

A

DNA methylation, xsomal instability, telomerase activation

48
Q

severe dysplasia assoc w

A

incr gene exp of E6 E7 which interfere w p53

49
Q

what does p53 do

A

mediate if a cell is stable enough to undergo cell prolif or should be marked for apoptosis

50
Q

viral interence of cell host mechs. dna integration interrupts what

A

E2 ORF

51
Q

site of integration is often

A

xsomal fragile

52
Q

expression of E2 does what

A

downregulate E6, 7

53
Q

E6, 7 ~results in ubiquitination of

A

p53 & pRB (retinoblastoma tumor suppressor protein)

54
Q

loss of cellular p53& pRB allows cell w dna damage to

A

divide, incr risk of cancer development

55
Q

hpv infection, progression. virus disrupts ?

A

cell cycle control, promote uncontrolled cell div & accum gene damage.

56
Q

cervical intraepithel dysplasia

A

pre-malignant transform & abnormal growth of squamous cells on cervix surface

57
Q

CIN cervical intraepithelial neoplasia is a cancer?

A

NO. it’s usually curable

58
Q

CIN 1, 2, 3

A

1 - mild dysplasia (HPV infection)
2 - moderate
3 - severe dysplasia/carcinoma in situ (integrate HPV genome, upregulate viral oncogenes)
… invasive carcinoma

59
Q

progression of cervical disease after HPV infection

A

ASCUS/LSIL - HPV infection koliocytosis/CIN1.

HSIL - CIN2/3.

60
Q

innate immune system (1st line of defence)

A

does NOT prevent HPV entry

61
Q

HPV E6, 7 implicated in

A

inhib TLR9 (dsDNA) gene transcription

62
Q

HPV has unique evasion mech to

A

replicate undetected by immune system

63
Q

HPV downregulates

A

interferon regulatory genes (dampening immune responses)

64
Q

HPV upregulates

A

TGF-b

65
Q

what is TGF-b

A

potent immuno-modulator. quench immune activation

66
Q

HPV infection does not elicit danger signals which would lead to

A

activation/trafficking of APCs & immune cells

67
Q

HPV NOT a cytolytic virus since

A

causing cell death would be potent immune activator

68
Q

HPV NOT assoc w viremia so

A

inflammatory markers not activated

69
Q

E5 protein does what

A

inhib acidification of endosomes & downregulate MHC class I expression

70
Q

MHC class I

A

impact immune recognition by CD8+ T cells

71
Q

incr viral protein exp only occurs in

A

keratinocytes, avascular areas (limited access for immune system)

72
Q

2 licensed vaccines on market

A

gardasil (9 valent) & cervarix (bivalent for types 16, 18)

73
Q

how is gardasil & cervarix made?

A

recomb tech. proteins form VLPs virus like particles of L1 protein (non-infectious, lack live biological prods)

74
Q

major basis of protection against infection

A

neutralize serum IgG that transudates from capillaries to genital epithel mucosa & binds to viral particle

75
Q

up to 1 yr after dose 1, HPV16 & 18 antibodies in cervicovaginal secretions & serum are

A

strongly correlated

76
Q

efficacy against combined endpoint of CIN1, CIN2/3 due to HPV 6, 11, 16, or 18

A

of 96% or + efficacy (up to 3.7 yrs after vaccination for F 15-26) … similar efficacy for bivalent vaccine in HPV 16 & 18

77
Q

australian surveillance cohort

A

funded HPV vaccination for 12-13, catch up programs for 13-26 girls, women & men showed decr in genital warts … cervical cancer vaccine may eradicate disease

78
Q

new 9 valent vaccine found to be

A

equivalent/non-inferior to quadrivalent HPV vaccine (but covers more serotypes)

79
Q

HPV seropositivity rises a lot as

A

15-21 ppl become sexually active

80
Q

most HPV infections are

A

asymptomatic, cleared by immune system.

81
Q

small proportion of HPV infections can

A

progress to cerv cancer

82
Q

development of cancer linked to

A

ability of virus to disrupt normal cell cycle control, promote uncontrolled cell div & accum genetic damage

83
Q

hpv genotypes divided into

A

diff risk groups, stratified according to oncolytic properties

84
Q

hpv vaccine elicits

A

IgG immune response

85
Q

evidence of hpv efficacity >95%

A

clin trial data & post vaccine surveillance cohorts, australia

PATH310 (8 decks)

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