Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Parasitology/Virology > Papilloma & Polyoma > Flashcards

Papilloma & Polyoma Flashcards

1
Q

What are common characteristics of Papillomaviruses and Polyomaviruses?

A
  • Non-enveloped, small icosahedral capsid viruses
  • double stranded circular DNA genome
  • Uses host polymerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two major polyomaviruses?

A

JC virus and BK virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the mode of transmission of polyomaviruses?

A

Respiratory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What regions are encoded by the polyomavirus genome?

A

Early, late, and non-coding regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do the polyomavirus early gene regions encode?

A

Non-capsid regulatory proteins: Large-T antigen, small-T antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the function of large T antigen?

A

Binds and inactivates p53 and Rb protein (tumor suppressor proteins, therefore has potential to cause cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do the polyomavirus late gene regions encode?

A

VP1, VP2, VP3 structural proteins (capsid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the most common clinical presentation of polyomavirus?

A

Asymptomatic!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In what population will you see clinical disease due to polyomavirus?

A

Immunosuppressed

  • HIV patients (CD4 <200)
  • Transplant patients
  • Monoclonal antibody therapy (natalizumab, rituximab)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the main target organ for primary viremia of polyomavirus?

A

Kidney (usually remains latent indefinitely in kidney unless reactivated by immunosuppression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the clinical manifestation of JC virus?

A

Progressive multifocal leukoencephalopathy (PML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the pathogenesis of PML?

A

JC virus infects oligodendrocytes and astrocytes, causing characteristic demyelinating lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the clinical manifestation of BK virus?

A

Polyomavirus-associated nephropathy and ureteral stenosis

Hemorrhagic cystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which types of HPV are high risk (higher potential for maliganant progression)?

A

16 and 18 most prevalent

Also 31, 33, 45, 52, 58

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which types of HPV are low risk (usually cause benign papillomas aka warts)?

A

6 and 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What population acquires most new infections of HPV?

A

15-24 year olds

17
Q

What is the mode of transmission of HPV?

A

Vaginal/anal/oral intercourse and genital contact

Rare nonsexual transmission: mother to newborn, fomites

18
Q

How does the capsid size and genome size of HPV compare to that of polyomavirus?

A

Slightly bigger
HPV: capsid = 55 nm, genome = 8 kb
Polyoma virus: capsid = 40 nm, genome = 5 kb

19
Q

What regions are encoded by the HPV genome?

A

Long control region (LCR), early region, and late region

20
Q

What does the early genome region of HPV encode?

A

Genes for replication and HPV viral oncogenes (E6 and E7)

21
Q

What does the late genome region of HPV encode?

A

L1 and L2 = structural genes that form the capsid

22
Q

What is the life cycle of HPV?

A
  • Accesses basal cell layer of epithelium through microtrauma to mucosa or skin
  • HPV interacts with integrins and gets engulfed
  • Exists episomally in basal cells
  • Early genes stimulate cell growth, facilitating replication of viral genome by host DNA polymerase when cells divide
  • Virus induced increase in cell number causes basal layer and stratum spinosum to thicken (wart or papilloma)
  • As basal cell differentiates, factors expressed in different layers of skin promote transcription of different viral genes (late genes expressed only in terminally differentiated upper layer)
23
Q

How does HPV become malignant?

A

Viral DNA gets integrated into host DNA, causing a loss of E2
Without E2, get consitutive activation of HPV viral oncogenes E6 and E7, causing increased proliferation and decreased repair of secondary mutations

24
Q

What is the function of E6?

A

Degradation of p53 tumor suppressor

25
Q

What is the function of E7?

A

Degrade Rb proteins (normally control cell cycle entry)

26
Q

What is clinical presentation of low risk types of HPV 6 and 11?

A
  • Warty lesions, usually perianal or penile
  • If contracted from birth canal, get recurrent respiratory papillomatosis
  • Cervical/anal intraepithelial neoplasia grade 1 (mild)
27
Q

What is clinical presentation of high risk types of HPV 16 and 18?

A
  • Cervical/anal intraepithelial neoplasia grade 2 or 3 (moderate or severe)
28
Q

How is HPV diagnosed?

A

Molecular detection of RNA/DNA = gold standard

Obtain specimen from pap smear or directed biopsy

29
Q

What is treatment for HPV?

A

Infection does not require treatment, cellular changes associated with infection require treatment

  • Observe at low grade abnormality
  • Surgery and ablation of affected tissue and high grade abnormality
30
Q

What are the two types of HPV vaccine?

A

Bivalent

Quadrivalent

31
Q

What is the HPV vaccine composed of?

A

Recombinant DNA-generated L1 proteins that self-assemble into viral like particles (VLPs)
VLP is like empty shell of HPV

32
Q

Which HPV vaccine is licensed for use in males?

A

Quadrivalent

Parasitology/Virology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions