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HPV Flashcards

1
Q

HPV belongs to what family of viruses?

A

papillomaviruses

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2
Q

describe the structure of HPV

A
  • small
  • non-enveloped
  • ds dna virus
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3
Q

how is HPV transmitted generally?

A
  • through sexual contact / close personal touching
  • # 1 STD globally
  • most prevalent STD in the us
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4
Q

is HPV a family of viruses or a single subset?

A
  • family

- 100s have been identified

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5
Q

what is the clinical presentation of HPV?

A
  • majority = asymptomatic
  • gentical warts = most common symptom
  • cervial dysplasia can also occur - precursor for cervical cancer which can occur if left untreated
  • other cancers can also occur but are less common (head/neck, anal, penile)
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6
Q

who experiences the majority of the HPV disease burden, men or women?

A

women

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7
Q

what would is indicated by a patient who has antibodies for HPV but receives a negative PCR test? what are the limitations of such a result?

A
  • indicates that the person has been exposed to HPV at some point in their live
  • but it does not dictate whether an infection has happened, if an infection has occured in the past or if an infection is currently present
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8
Q

what are the risk factors for cervical cancer? (5)

A
  • lack of effective screening
  • smoking
  • multiparity (multiple kids)
  • long-term use of oral contraceptives
  • HPV
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9
Q

what are the risk factors for HPV? (6)

A
  • age
  • sex
  • lack of condom use
  • age of first inercourse/number of partners
  • not beign circumsized
  • co-infections (especiallly if other STIs)
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10
Q

why is age a risk factor for hpv?

A
  • maturation of cervical mucosa

- cells that compose the cervix change as women mature (younger cells are most susceptive to HPV)

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11
Q

why does circumcision reduce the risk for hpv?

A
  • the foreskin cells are sesceptible to hpv

- there is less surface area which decreases the risk of spreading

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12
Q

how is hpv transmitted specifically?

A

through endothelial cells not liquids

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13
Q

what is the natural cycle of an hpv infection? are all of these steps reversible?

A

normal cervix => hpv infection => initiated cancer => benign tumor => malignant tumour
-all are reversible except from benign to malignant

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14
Q

where does “regression” occur in the hpv cycle?

A

from initated stem cell cancer back to hpv infection

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15
Q

where does “clearence” occur in the hpv cycle?

A

from hpv infection to normal cervix

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16
Q

describe the anatomy of the cervix

A

composed of 3 sections:

  • external os: opening to vagina (stratified squamous)
  • endocervical canal (glandular epithelium)
  • internal os: opening to uterus (stratified squamous)
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17
Q

what is the transformation zone?

A

area of the cervix where the squamous epithelium of the external os meets the glandular epithelium of the endocervical canal

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18
Q

what is the significance of the transformation zone with respect to hpv?

A

this is the area where hpv infects susceptible cells

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19
Q

what are the 3 possible outcomes after hpv infection of the transformation zone?

A

(1) clearance: the majority of infections result in viral clearance within 2 years of the infection
- immune system is engaged
(2) persistance: infection does not clear on its own
- hpv tethers itself to host dna and continuously repiicates at low levels building up a reserve
- the immune system is not engaged
(3) progression: small portion progress to initiated cervical cancer stem cells

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20
Q

describe initiated cervical cancer stem cells

A
  • these cells have undergone genetic transformation as a result of the hpv infection
  • are able (if left unchecked) to generate a benign cervical tumor
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21
Q

viral gene expression of the hpv genome is thought to be related to:

A

the state of differentiation of the infected epithelium

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22
Q

describe microabrasions as a mechanism for hpv infection

A
  • sexual intercourse causes microtears within the genital tract due to friction
  • hpv uses these as a portal of entry
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23
Q

what are basal keratinocytes

A
  • hpv travles down and infects these
  • these are the cervival cells at the layer farthest from the lumen
  • from here there are two equally possible ways the virus can continue the infection process
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24
Q

define viral assembly as one of the 2 possible processes of hpv infection

A
  • differentiation of hpv infected cells
  • as infected keratinocytes differentiate they move up towards the mucosa bringing the virus with them
  • the virus enters different stages of gene expression
  • when they reach the lumen, the virus has assembled and is infectious
  • virus is released into surrounding tissues spreading the infection
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25
Q

does viral assembly usually lead to hpv-mediated cancer?

A

no

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26
Q

where do the different stages of gene expression occur during viral assembly?

A

(1) suprabasal layer

(2) terminal karatinocyte

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27
Q

what is the type of gene expression associated with the suprabasal layer?

A

early stages: producing proteins that encode for viral dna

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28
Q

what is the type of gene expression associated with the terminal keratinocyte

A

late stages: producing proteins that encode for structural proteins

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29
Q

explain chromosomal integration as one of the 2 possible processes of hpv infection

A
  • the virus integrates its genome into the host dna

- this can result in uncontrollable oncoprotein production and host cell transformation

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30
Q

does chromosomal integration usually lead to hpv-mediated cancer?

A

yes

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31
Q

can chromosomal integration and viral assembly happen at the same time?

A

yes

32
Q

what is the mechanism of persistance for hpv? what is the result of this?

A
  • chromosomal integration - disrupts normal cell cycle leading to uncontrolled cell division and the accumulation of genetic damage
  • this damage can lead to cervical dysplasia (endothelial lesions) and abnormal growth of squamous cells on the cervix
  • this is a premalignant transformation
33
Q

is cervical intraepithelial dysplasia curable?

A

yes

34
Q

what genes are associated with severe dysplasia?

A

E6 and E7 hpv oncoproteins

35
Q

what is the function of the E7 protein?

A
  • inhibits pRB to stop cell cycle arrest

- i.e. this is the primary transforming protein that facilitates the proliferation of disregulated cells

36
Q

what is the function of the E6 protein?

A
  • interferes with the normal function of p53 (decides if cells should be marked for apoptosis - usually would happen if too many were produced (E7))
  • allows for further cell disregulation
37
Q

what are the hpv genotypes for patients with low risk of hpv

A

6, 8, 11

-genital warts

38
Q

what are the hpv genotypes for patients with probable high Irisk of hpv

A

26, 53, 66

-precancerous lesions

39
Q

what are the hpv genotypes for patients with high risk of hpv

A

16, 18

-cervical cancer

40
Q

what can explain the higher risk subtypes of hpv?

A

oncoproteins (E6/E7) have a higher binding affinity for the p53 and pRB proteins and are therefore more disruptive to cells

41
Q

_____ might be an important biomarker for distinguishing hpv infection from benign tumors?

A
  • it has been observed that the hpv genome is integrated into host cell dna in a high portion of patients with high grade carcinoma
  • not necessary for integration though
42
Q

describe how progression of the hpv infection can result in cervical cancer

A
  • accumulation of endothelial cells disrupts the organized structural appearance of epithelial tissue
  • disorganization extends through the upper layers and to the surface of the epithelium
43
Q

what is used to classify the degree of a cervial lesion?

A

progression of abnormal cell growth

44
Q

what are the requirements for CIN1?

A

abnormal cell growth in the lower 1/3 of the cervical endoethium

45
Q

what are the requirements for CIN2?

A

abnormal cell growth in the lower 2/3 of the cervical endoethium

46
Q

what are the requirements for CIN3?

A

abnormal cell growth >2/3 above the basal membrane

47
Q

what is the intermediate precursor to cervical cancer?

A

CIN3

48
Q

when does invasive cancer ensue? (when does it become the ultimate consquence)

A
  • when the abnormal cells break through the basal membrane and infect the dermis
  • when it gets to the basal membrane the virus sheds its capsid and the viral dna enter host cell
  • this is where E6 and E7 take action
  • result is a worse phv infection and cervical cancer
49
Q

what gene is used to identify hpv?

A

L1

50
Q

what are key steps in preventing cervical cancer? (5)

A
  • screening (pap smear)
  • triage results (bethesda screening system triages results from pap smear)
  • colposcopy - used to get a closer look at concerning results
  • treatment
  • post-treatment follow up
51
Q

describe screening tests used for hpv and why they are useful

A
  • progression of hpv is linked to histologic and cytologic appearance of the cervical tissue
  • histology = study of the entire tissue (can be invasive)
  • cytology = study of isolated tissue (very effective for early stage detection)
  • both have similar classification systems
52
Q

describe a pap smear procedure

what are the advantages of this method?

A
  • involves the use of a cervical brush to scrape surface mucosal cells off of the cervix
  • these cells are then immediately smeared onto a slide or swirled in alcohol and then dispensed onto slides to be analyzed for precancerous changes
  • relatively cheap and quick
53
Q

what is the purpose of the brethesda screening system?

what are the possible results?

A
  • interprets pap smear results
  • the system has standardized diagnostic categories for the different stages of cervical cancer
  • results can be either:
    (1) normal squamous mucosa
    (2) atypical squamous cells of undetermined significance
    (3) low grade squamous intraepithelial lesion
    (4) high grade squamous intraepithelial lesion
    (5) carcinoma
54
Q

describe normal sqamous mucosa

A
  • no evidence of abnormal cells

- basal cells are maturing into healthy epithelium

55
Q

describe atypical squamous cells of undetermined significance (ASCUS)

A
  • mild atypia but not quite LSIL
  • nuclei are mildly enlarged
  • no suggestion of perinuclear clearing
56
Q

describe low grade squamous intraepithelial lesion (LSIL)

A
  • nuclei are enlarged and dark with perinuclear clearing
  • may be binucleated
  • begining of hpv infection
  • cells are infected but not pre-malignant tumors
57
Q

describe high grade squamous intraepithelial lesion (HSIL)

A
  • loss of clearing with busy looking epithelium because each cell has more nucelus than cytoplasm
  • indicated the infection has been present for an extended period of time
  • pre-malignant and will likely progress to carcinoma
58
Q

describe carcinoma

A
  • hpv infected cell has progressed to an invasive squamous cell carcinoma
  • viral dna is integrated into host cell dna
  • normal regulation has been altered
  • cells may not resemble normal structure at all
59
Q

what is the traditional method for management of ASCUS or LSIL results?

A

the individual will be sheduled to repeat the pap smear in 6 months and is referred to a colposcopy

60
Q

what is the traditional method for management of HSIL or carcinoma results?

A

indivdual is sent to colposcopy

61
Q

how long does the progression from CIN1 - CIN2 or from CIN2 - CIN3 take?

A

months

62
Q

how long does the progression from CIN3 - carcinoma take?

A

years

63
Q

how is hpv able to stay under the radar of the immune system? (5)

A
  • doesnt lead to apoptosis (usual trigger for immune response)
  • replicates cells without altering them to much
  • has proteins that shut down the innate immune response -delays the adaptive response
  • downregulates th1 and th2 to supress the adaptive immune response
64
Q

describe the process of a colposcopy

when is this preformed?

A
  • preformed when theres concerning pap smear results

- gynecologist uses a colposcope (special microscope) to magnify the cervix for better visualization of the tissue

65
Q

what happens if there are abnormal areas identified during the colposcopy?

A

gynecologist will biopsy the tissue, which is sent to path where it is analyzed to confirm the presence of hpv or cervical cancer

66
Q

what do treatment methods depend on?

A

biopsy results

67
Q

define cryotherapy

A
  • surgical procedure used to freeze an destroy abnormal cervical tissue
  • speculum is inserted into vagins, cyroprobe with nitrogen gas is used to freeze the tissue
  • dead cervical tissue then sheds in the following weeks
68
Q

define loop electrosurgical excision procedure (LEEP)

A
  • loop of electrical wire is passed through the cervical os to remove a half donut-shaped piece of cervical tissue
  • this tissue is then sent to path
69
Q

define cold knife cone biopsy

A

a scalpel is used to exise the abnormal tissue

70
Q

what are the preffered treatments? why?

A
  • LEEP and cold knife

- bc physicians have clear margins and can ensure the abnormal tissue is removed

71
Q

what is the post-treatment follow up for cryotherapy, LEEP and cold knife cione biopsy?
what happens if results are normal?

A
  • colposcopy and a pap smear

- if results are normal the patient returns to routine screening

72
Q

compare and contrast the test for the presence of hpv dna from collected cervical cells and a pap smear

A
  • checks for the presence of viral dna where the pap smear checks for morphological changes to the cervical epithelial cells
  • not covered by ohip, faster
  • beneficial for confirming if suspicious results are truly abnormal
  • can also be used to indicate hpv post-treatment
73
Q

how are the hpv vaccines made? are they non-infectious? why or why not?

A
  • with recombinant technology
  • virus like particles of the L1 protein are inserted into recombinant plasmid
  • non-infectious - lack live particles
74
Q

can hpv vaccines provide protection of you are already exposed?

A

no

75
Q

describe Gardasil

A
  • 2006
  • first protected against hpv 6,8,18 and 18
  • now protects against 9 types
76
Q

describe Ceravix

A
  • 2010
  • females btwn 9 and 45
  • hpv 16,18

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