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Medical virology > Papillomaviruses > Flashcards

Papillomaviruses Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the origins of Papilloma viruses thought to be?

A
  • changes in the epithelium of reptiles millions of years ago
  • coexisted with their hosts for along time so co-evolved, explaining why they often cause no or very mild symptoms (warts)
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2
Q

Which genera of papilloma virus infects humans?

A
  • alpha papilloma virus
  • akak human papillomavirus HPV
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3
Q

Describe the HPV virion

A
  • small and non-enveloped
  • has a capsid built from 72 pentameric capsomer subunits which is more resistant to destruction than an envelope
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4
Q

Describe the structure of the HPV genome

A
  • contains a long control region (LCR)
  • 8 genes spliced into a larger number of gene products
  • 6 early (E) genes and 2 late (L) genes
  • size and position of the major ORFs differs between HPV strains
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5
Q

What are the roles of HPV early genes E1 and E2?

A

viral DNA replication alongside host DNA replicationW

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6
Q

What are the roles of HPV early genes E3 and E8?

A

these are putative genes seen only in some HPV strains

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7
Q

What are the roles fo HPV early genes 4 + 5?

A

neede for amplification of the viral genome in the upper layers of the host epithelium

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8
Q

What are the roles of HPV early genes E6 and E7?

A

are oncogenic in high-risk HPVs - immortalise and genomically stabilise cells

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9
Q

What are the roles of HPV late genes L1 + L2?

A

form the viral capsid when in the upper host epithelium

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10
Q

What is the role of HPV LCR?

A

contains regulatory sequences needed for viral genome replication and expression

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11
Q

How does HPV replicate in host cell?

A
  • attachment and entry (basal epithelium)
  • uncoating and genome entry (circular dsDNA)
  • replication and transcription (by host machinery)
  • late gene expression and capsid formation
  • assembly and release (cell lysis)
  • infection of adjacent cells
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12
Q

How do HPV cells enter the epithelium and how is it maintained/regulated there?

A
  • micro-wounds/lesions allow cells to acess the basal lamina and infect
  • can be maintained in low copy number episomes in these less differentiated cells
  • as the cells move upwards and begin to differentiate the virus begins to replicate and express late genes to produce new HPV virions in terminally differentiated cells
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13
Q

How can HPV persistently infect epithelial cells?

A
  • at the basal lamina
  • increased E6 and E7 expression
  • can cause the formation of pre-cancerous lesions
  • viral load is highest at this precancerous state
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14
Q

What kind of epithelial cells can HPV infect?

A

infect squamous epithelial both cutaneous and mucosal. infection of mucosal epithelium can be more invasive and dangerous

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15
Q

Which HPVs are associated with which outcomes?

A
  • 30 HPVs associated with genital warts and growths
  • 15 associated with cervical cancer
  • HPV-18, 16 and 33 make up 70% of this
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16
Q

How is HPV transmitted?

A
  • sexual contact
  • mostly sexual intercourse
17
Q

What is the significance of HPV-16 and HPV-18 in cervical cancer?

A
  • the only HPVs that can give rise to immortalised cell lines
  • co-operate with ras oncogenes
  • HPV association with cancer is stronger than that of smoking
18
Q

Where is HPV most common?

A
  • in low-middle-income countries with less education and vaccination
19
Q

Give some stats on cervical cancer (2)

A
  • 52% mortality
  • 7% of women with HPV-16 will develop cervical cancer within 45 years of infection
20
Q

Name 3 risk factors/ cofactors for cervical cancer

A
  • smoking
  • age at first intercourse
  • number of sexual partners
21
Q

What are the major steps of cervical cancer development?

A
22
Q

What features of HPV allow for presistent infection?

A
  • E5, E6 and E7 have roles in immune evasion
  • viral gene expression is shut off in the presence of infiltrating lymphocytes but viral episomes are not effectively cleared from the basal cell layer
23
Q

How does HPV genome DNA integration lead to cancer?

A
  • integration into the genome carries a risk in itself as it can cause genomic instability
  • HPV integration specifically can interrupt E2 expression and reduce downregulation of oncoproteins E6 and E7
24
Q

What cellular processes can HPV E6+E7 interfere with to cause cancer?

A
  • E6 interferes with p53 and activates telomerase
  • E7 maintains telomeres and modulates cell cycle progressionH
25
Q

How does HPV E6 interfere with p53?

A
  • associates with E6qp and causes the degradation of p53 allowing the cell cycle to progress even with incorrect DNA or cell damage
26
Q

How does HPV E7 modulate cell cycle progression?

A
  • targets Rb for degradation or sequesters it
  • E2F is free to bind to the DNA allow passage through the cell cycle
27
Q

How do HPV E6+E7 activate and maintain telomeres in cervical cancer?

A
  • E6 activates telomerase reverse transcriptase (TERT)
  • E7 maintains telomere length through the alternative pathway
  • E7 is more important in early cancer and E6 in later cancers
28
Q

What is the key difference between E6+E7 in high risk and low risk HPVs?

A
  • in low risk is induces cell entry
  • in high risk it induces cell entry and immortalisation of cells and can bind to and interact with p53 and Rb
29
Q

How do we know that immunity plays a key role in the regression of HPV?

A
  • warts more common in those under immunosuppression and can regress when suppression is lifted
  • precancerous lesions are much more common in AIDs patients
  • antibodies to the L1 protein are seen in those with genital warts
30
Q

What are HPV L1 vaccines?

A
  • destroy the L1 outer capsid and prevents the virus from entering the cells in the first place
  • in clinical trials
  • shown sucesses in musocal dog papillomavirus
31
Q

What vaccine against HPV does exist? Has it worked?

A
  • Gardasil given to girls 9-12
  • 90% reduction in HPV infection of targetted strains
  • 85% reduction in high-grade abnormalities
  • beginning to vaccinate boys to further reduce the spread
32
Q

What are some important factors to consider when designing new HPV vaccines?

A
  • protective against multiple strains
  • protects against other HPV-associated cancers
  • duration or level of cancer protection
  • accessible and affordable to lower-income countries where 80% of disease burden lays

Medical virology (15 decks)

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