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MIMM 324 > 9. Papillomavirus 1 > Flashcards

9. Papillomavirus 1 Flashcards

1
Q

describe the papillomavirus structure and genome. is it enveloped or naked?

A

dsDNA virus in an icosahedral capsid

naked

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2
Q

what is the family of papillomavirus?

A

papillomaviridae

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3
Q

what baltimore class is papilloma?

A

class I (dsDNA)

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4
Q

what cells does papilloma infect?

A

infects keratinocytes with differentiating epithelia in skin and mucosa

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5
Q

what does the papilloma life cycle depend on?

A

depends on the differentiation program that keratinocytes undergo in the epithelia

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6
Q

what is unique about how papilloma affects cells?

A

papilloma must infect cell AND induce differentiation

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7
Q

what type of lesions does papilloma cause?

A

hyper-proliferative benign or malignant lesions of skin and mucosa

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8
Q

how many types of papilloma virus are there? what is different between them?

A

there are >200 types, each with a preference for certain anatomical locations

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8
Q

how was papilloma first discovered?

A

made extract of common warts and infected human subjects –> they got warts

then found that cell-free filtrate of common warts can transfer infection

therefore, warts are caused by a virus

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9
Q

how was the oncogenic potential of papillomavirus discovered?

A

cottontail (wild) rabbits were found to have lesions from papillomavirus –> made extract of these lesions and infected domestic rabbits –> caused malignancy

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9
Q

when was HPV first associated with cervical cancer?

A

in 2008

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10
Q

other than those 3 genuses, what type tissue do all other genuses infect?

A

cutaneous

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10
Q

what are 3 genuses of papillomaviruses? what type of tissue do they infect?

A
  1. Genus ALPHA –> cutaneous and mucosal
  2. Genus BETA –> cutaneous
  3. Genus GAMMA –> cutaneous
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10
Q

what 2 genuses most commonly cause lesions?

A

beta and gamma

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11
Q

what genus causes cancer?

A

MUCOSAL alpha genus

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12
Q

what determines different HPV types?

A

if the L1 open reading frame is >10% different than other known types, it is a new type

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13
Q

what determines different HPV variants?

A

if the L1 open reading frame is <10% different than other known types, it is a new variant which can still have significant effects (sometimes more than different types)

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14
Q

how is mucosal HPV transmitted?

A

sexually

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15
Q

what are 4 results of mucosal HPV?

A
  1. cervical and anogenital cancers
  2. oropharyngeal cancers
  3. genital warts
  4. laryngeal papillomas
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16
Q

what type of HPV are cervical and anogenital cancers caused by?

A

HIGH-RISK types –> HPV16, 18

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17
Q

what type of HPV are genital warts and laryngeal papillomas caused by?

A

LOW-RISK types –> HPV6, 11

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18
Q

are HPV cancers hard to treat?

A

no they respond well to radiation

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19
Q

how do oropharyngeal cancers from HPV compare to oropharyngeal cancers from other causes (alcohol, smoking)?

A

HPV oropharyngeal cancer is more common nowadays but easier to treat than orophrayngeal cancer from other causes

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20
Q

what is layngeal papillomas? what is it caused by?

A

lesions in throat of young children

due to newborn being infected by an infected mother during vaginal birth

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21
Q

how are cutaneous HPVs transmitted?

A

by contact

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22
Q

what are the 3 things that cutaneous HPV causes?

A
  1. plantar warts
  2. common warts
  3. flat warts
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23
Q

what type of HPV causes plantar warts?

A

HPV1

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24
Q

what type of HPV causes common warts?

A

HPV 2,4,29

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25
Q

what type of HPV causes flat warts?

A

HPV 3,10,28,49

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26
Q

do all HPVs cause cancer?

A

no, only high risk HPV

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27
Q

what is the only genetic predisposition we know of for HPV?

A

epidermodysplasia verruciformis

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28
Q

what is epidermodysplasia verruciformis (EV)?

A

rare genetic disease characterized by higher risk for skin carcinoma on sun-exposed skin due to higher sensitivity to specific HPVs

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29
Q

what type of HPV are EV patients susceptible to?

A

BETA-HPVs like HPV5 and HPV6 that are present in the skin

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30
Q

how do beta-HPVs affect normal ppl vs EV ppl?

A

normally sit in the skin and don’t cause any mutations but EV ppl develop cancer

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31
Q

what causes EV?

A

mutations in EVER1, EVER2, and CIB1 genes

32
Q

why are EV patients susceptible to beta-HPV?

A

normally, EVER1, EVER2, and CIB1 proteins form a complex involved in the innate immune response of keratinocytes to beta-HPVs

in EV patients, this response is lost –> become susceptible to beta-HPV

33
Q

What is one of the most common STIs?

A

HPV

34
Q
  • who can be infected with HPV?
  • what % of women are infected in their lifetime?
  • what is the average length of infection?
  • are all infections diagnosed?
A
  • both men and women can be infected
  • 50-70% of women are infected during their lifetime
  • normally lasts 8-12 months
  • most infections not diagnosed!
35
Q

describe the progression of HPV infection

A
  1. inoculation
  2. incubation for 1-8 months
  3. first lesion develops and virus proliferates
  4. immune response begins
  5. 6-8 months after first lesion, either will go into remission or infection will persist
36
Q

what determines whether infection will persist or go into remission?

A

we don’t know! there isn’t a genetic factor that determines this

37
Q

what percent of people have cervical dysplasia?

A

4%

38
Q

what percent of people have condylomas?

A

1%

39
Q

what are condylomas?

A

benign genital wart

40
Q

what percent of people have viral nucleic acids (DNA or RNA) found via PCR?

A

10%

41
Q

What percent of people have antibodies to HPV capsid proteins?

A

60%

42
Q

why do most people have have antibodies to HPV capsid protein?

A

bc virus is everywhere –> we’ve been able to mount an effective immune response

42
Q

what percent of people have no sign of prior or active infection?

A

25%

43
Q

what is the purpose of HPV screening?

A

to identify cervical lesions that could progress or have progressed to cancer

44
Q

what is a PAP test?

A

cytological test to look at abnormal keratinocytes in cervical tissue

45
Q

describe molecular detection of HPV

A

PCR of PAP sample can detect viral nucleic acids (DNA/RNA), mainly high-risk HPV

46
Q

when do HPV patients get colposcopy?

A

if PAP test is abnormal and high-risk HPV nucleic acids are present –> must perform colpsocopy

47
Q

what is colposcopy?

A

direct visualization of lesions from biopsies for histology, often coupled with treatment

48
Q

how can you visualize HPV lesions in cervix?

A

bathe cervix with vinegar, lesions turn white

49
Q

what are 3 treatments for HPV?

A
  1. physical ablation
  2. cytotoxic agents
  3. immunomodulation
50
Q

what antiviral drugs are used for HPV?

A

no antiviral drugs are available

51
Q

what is an example of an immunomodulation agent?

A

Imiquimod

52
Q

what is Imiquimod used for?

A

benign genital warts

53
Q

what does imiquimod do?

A

cream to stimulate cells to make certain cytokines to fight against

54
Q

what are vaccines made of?

A

virus-like particles VLPs made by expression of L1 in yeast or insect cells

55
Q

how does L1 form virus-like particles?

A

self-assembles into capsid-like particles to trigger immune response

56
Q

what are the 3 HPV vaccines?

A
  1. Cervarix
  2. Gardasil
  3. Gardasil 9
57
Q

why are there multiple HPV vaccines?

A

because antibodies for 1 type won’t protect from other type, need to target multiple HPV types

58
Q

what is the role of HPV vaccines?

A

to provide high levels of antibodies to protect against cervical cancer and condylomas

59
Q

what does the papillomavirus contain?

A

1 viral genome wrapped in histones

60
Q

why is the papilloma genome wrapped in histones?

A

bc genome comes from nucleus of the host

61
Q

what is the symmetry of papillomavirus?

A

icosahedral

62
Q

what is the T number of papilloma?

A

7

63
Q

describe the pentamers and subunits of papilloma capsid

A

72 pentamers of L1 which interact thru long tails for stability –> 360 subunits

NO HEXAMERS

64
Q

what makes papillomavirus different from other T=7 virus?

A

capsid of papilloma has 360 subunits, other T=7 viruses have 420 subunits (missing 60 subunits bc would make up hexamers normally [T-1]10 = 60)

65
Q

describe L2
- how many copies?
- location

A

12 copies of minor capsid protein L2 are on the inside of the capsid and may help with packaging the genome

66
Q

describe the cryo-EM structure of the HPV capsid

A
  • 72 L1 pentamers
  • 12 pentamers surrounded by 5 neighbours
  • 60 pentamers surrounded by 6 neighbours
67
Q

what percent of HPV-associated cancers are cervical cancers?

A

80%

68
Q

how does the incidence of cervical cancer correlate to access of cervical screening programs?

A

less cervical cancer when more access to screening

69
Q

describe the presence of oropharyngeal cancers in high-income countries

A

incidence of cancer is increasing in high-income countries but the total number of cases remains small

70
Q

what does virus infect? what does it lead to?

A

virus infects undifferentiated basal cells but produces new virions in differentiated cells

71
Q

describe the entry of papilloma in basal cells

A

L1 binding to heparan sulfate proteoglycans triggers clathrin-dependent endocytosis

72
Q

describe the genome of papilloma in basal cells in basal cells

A

genome is established as an episome in the nucleus and replicated by E1 and E2 to 50-100 copies –> not integrated in genome, remain as episome

73
Q

what are the 5 steps of papilloma lifecycle in a differentiation epithelium?

A
  1. infection of basal cells
  2. oncogene-induced cell proliferation
  3. genome amplification
  4. late gene/capsid protein expression
  5. packaging and release of virions
74
Q

what are the 2 oncogenes in papilloma?

A
  1. E7
  2. E6
75
Q

what is the role of E7?

A

E7 forces differentiated cells to enter S-phase

76
Q

what is the role of E6?

A

E6 prevents their death by apoptosis

77
Q

what occurs during oncogene-induced cell proliferation?

A
  1. E7 forces differentiated cells to enter S phase
  2. E6 prevents their death by apoptosis
  3. cells express host DNA replication factors
78
Q

what happens during genome amplification?

A

viral episomes are replicated by E1 and E2 to >1000 copies/nucleus

79
Q

what are 2 of the last genes to be expressed?

A
  1. L1
  2. L2
80
Q

how does papillomavirus grow in differentiating epithelium?

A

infects basal layers, then cells differentiate and virus releases by desquamation

MIMM 324 (37 decks)

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