Papilloma virus Flashcards

1
Q

PV genome: what does it contains

A

x5-6 Early (E) genes and x2 late (L) genes

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2
Q

How are PV classified?

A

Using L1 gene

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3
Q

PV life cycle

A

Microtrauma and transfer of PV to basal keratinocytes -E1+E2–> small copies that infect near by cells–> basal cell differentiates to subrabasal layer–>E6 +E7 prevents from terminal differentiation of cell ensuring the nucleus is retained forcing the epithelial cells to divide and make copies of the PV. –> Surface of peithelium L1+L2–>PV to the environment.

http://constiintaortodoxa.ro/images/831138.jpg

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4
Q

In what species PV has been associated with neoplasia

A

Horses(type 2), dogs, cats, cattle, pigs, sheep(type 3 in Ovine SCC, type 2 in a sarcoid like mass)

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5
Q

How histology can reveal PV infection?

A
  1. Intranuclear inclusions
    2.Cell changes
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6
Q

IHC against PV

A
  1. PV L1 antigen (this however, is produced in the late stages after viral replication. It is therefore detectable only when we have cell changes due to viral replication)
    ->no antibodies available against FcaPV
    Viral replication is rare amongst PV induced cancer (so PV L1 not that helpful)
  2. p16 (produced in PV induced cancer from degradation of pRB). p16 is not dependent on viral replication and therefore easier to detect in lesions
    –>spontaneous mutations in p16 and pRB may change amounts of p16
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7
Q

Sp and Se of p16 in cats and which clone?

A

unknown
clone G175-405

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8
Q

Papilloma types in cats

A
  1. FcaPV 1 –> oral and skin but mainly oral, and exotic felids
    2.FcaPV2–>DNA from skin of almost all cats, 1/3 of cats have ab against it, usually asymptomatic but can cause skin disease
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9
Q

PV degrades pRB and what happens?

A
  1. pRB degradion promotes cell divition
  2. accumulation of p16 which can be detected by IHC
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10
Q

WHich part of FcaPV binds to pRB?

A

E7
so FcaPV (the E7part) binds to pRB of the cell causing its degradation and therefore causes increased cell division(because pRB controls cell division)

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11
Q

What happens with p53

A

PV may influence neoplasia by degrading p53

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12
Q

What happens with UV light in a PV lesion?

A

In normal skin, most UV-induced DNA damageis repaired prior to cell replication. However, it is possible that when UV-induced DNAdamage occurs within a PV-induced lesion, the presence of the PV induces the cell toreplicate and inhibits apoptosis, predisposing to cancer development

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13
Q

FcaPV 3 and 4 and 5 and 6 classification

A

species 3 Taupapapillomavirus

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