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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
incr risk of HPV prevalence w what
other STIs (like HIV)
26
HPV types 16, 18 (high risk, lead to pre/cancerous lesions)
cause 70% cerv cancer cases (squamous cell)
27
HPV 6, 11 types (low risk, lead to condylomata acuminata)
cause 90% genital warts cases
28
HPV infection clin manifestations
cutaneous , anogenital warts. epidermadysplasia verruciformis. resp papillomatosis. other HPV infections
29
cutaneous warts
~asymptomatic, 50% resolve within 1 yr, rare but can degrade into carcinomas
30
anogenital warts
past history of anal warts, incr anal cancer 10x risk. vulvar condylomata acuminata
31
epidermadysplasia verruciformis
autosomal recessive genodermatosis linked to gene in xsome 17. appear in 1st decade of life, transformto invasive squamous carcinoma (malig)
32
respiratory papillomatosis
hoarseness. altered cry & resp fail, often for infants. obstruct trachea, lungs. require excision
33
other HPV infections
most common = oral squamous pappillomas. involve diff mucus membs (eyes, mouth)
34
HPV genome how many bps? ORFs which encode what proteins?
7900 bps, 8 ORFs - encode 6 early proteins, 2 late structural ones.
35
viral gene exp linked to differentiation state of infected epithel
suprabasal epithel cells - early gene exp. terminally differentiated karatinocytes - late gene exp.
36
HPV disease mech (aidasi)
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
most infections result in
viral clearance (mechs unclear), develop type-specific immune response
38
development of invasive cancer closely linked to
viral DNA integration
39
integration of viral dna leads to
overexpress E6, E7 to target p53, pRB. which incr cell prolif, decr repair > mutations > CIN > invasive cervical cancer
40
in basal cells, HPV viral dna replic occurs where, in what fashion, at what rate?
in squamous epithel cells. episomal fashion. low rate. 50-100 copies/cell
41
infected basal cells enter what
suprabasal cell layer, assoc w incr exp of early, late proteins E4 5 6 7
42
viral assembly occurs in what cells
terminally differentiated epithel cells (exp of L1, L2 proteins)
43
what occurs after viral assembly
virions released into tissue, infection spreads
44
viral integration takes place where?
in small proportion of basal lamina cells
45
viral integration is important for?
develop malignant disease (but not sufficient)
46
integration of HPV genome into xsome leads to
uncontrollable oncoprotein prod, host cell transform
47
other mechs playing key role in cancer develop incl.
DNA methylation, xsomal instability, telomerase activation
48
severe dysplasia assoc w
incr gene exp of E6 E7 which interfere w p53
49
what does p53 do
mediate if a cell is stable enough to undergo cell prolif or should be marked for apoptosis
50
viral interence of cell host mechs. dna integration interrupts what
E2 ORF
51
site of integration is often
xsomal fragile
52
expression of E2 does what
downregulate E6, 7
53
E6, 7 ~results in ubiquitination of
p53 & pRB (retinoblastoma tumor suppressor protein)
54
loss of cellular p53& pRB allows cell w dna damage to
divide, incr risk of cancer development
55
hpv infection, progression. virus disrupts ?
cell cycle control, promote uncontrolled cell div & accum gene damage.
56
cervical intraepithel dysplasia
pre-malignant transform & abnormal growth of squamous cells on cervix surface
57
CIN cervical intraepithelial neoplasia is a cancer?
NO. it's usually curable
58
CIN 1, 2, 3
1 - mild dysplasia (HPV infection) 2 - moderate 3 - severe dysplasia/carcinoma in situ (integrate HPV genome, upregulate viral oncogenes) ... invasive carcinoma
59
progression of cervical disease after HPV infection
ASCUS/LSIL - HPV infection koliocytosis/CIN1. | HSIL - CIN2/3.
60
innate immune system (1st line of defence)
does NOT prevent HPV entry
61
HPV E6, 7 implicated in
inhib TLR9 (dsDNA) gene transcription
62
HPV has unique evasion mech to
replicate undetected by immune system
63
HPV downregulates
interferon regulatory genes (dampening immune responses)
64
HPV upregulates
TGF-b
65
what is TGF-b
potent immuno-modulator. quench immune activation
66
HPV infection does not elicit danger signals which would lead to
activation/trafficking of APCs & immune cells
67
HPV NOT a cytolytic virus since
causing cell death would be potent immune activator
68
HPV NOT assoc w viremia so
inflammatory markers not activated
69
E5 protein does what
inhib acidification of endosomes & downregulate MHC class I expression
70
MHC class I
impact immune recognition by CD8+ T cells
71
incr viral protein exp only occurs in
keratinocytes, avascular areas (limited access for immune system)
72
2 licensed vaccines on market
gardasil (9 valent) & cervarix (bivalent for types 16, 18)
73
how is gardasil & cervarix made?
recomb tech. proteins form VLPs virus like particles of L1 protein (non-infectious, lack live biological prods)
74
major basis of protection against infection
neutralize serum IgG that transudates from capillaries to genital epithel mucosa & binds to viral particle
75
up to 1 yr after dose 1, HPV16 & 18 antibodies in cervicovaginal secretions & serum are
strongly correlated
76
efficacy against combined endpoint of CIN1, CIN2/3 due to HPV 6, 11, 16, or 18
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
australian surveillance cohort
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
new 9 valent vaccine found to be
equivalent/non-inferior to quadrivalent HPV vaccine (but covers more serotypes)
79
HPV seropositivity rises a lot as
15-21 ppl become sexually active
80
most HPV infections are
asymptomatic, cleared by immune system.
81
small proportion of HPV infections can
progress to cerv cancer
82
development of cancer linked to
ability of virus to disrupt normal cell cycle control, promote uncontrolled cell div & accum genetic damage
83
hpv genotypes divided into
diff risk groups, stratified according to oncolytic properties
84
hpv vaccine elicits
IgG immune response
85
evidence of hpv efficacity >95%
clin trial data & post vaccine surveillance cohorts, australia

PATH310 (8 decks)

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