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Repro Micro > HPV > Flashcards

HPV Flashcards

1
Q

What is the papilloma virus limited to?

A

Epithelial cells of the skin and mucosa

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2
Q

What do the HPV’s cause?

A

Benign tumors (warts) that can lead to malignancy (mostly cervical, but also penila, anal, oral, and neck)

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3
Q

What age groups are warts seen on hands and faces of? age group of anogenital warts?

A

Children; adolescents and young adults

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4
Q

What HPV strains are the more prominent anogenital warts (condyloma) caused by? What should be noted about these in regards to cervical cancer?

A

HPV 6 or 11; they are low risk

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5
Q

Sub-clinical papilloma infections (SPI) are hard to detect, what strains are they caused by and what is their risk level?

A

HPV 16 and 18, high risk for cancer (required for the development of cervical cancer)

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6
Q

What two proteins play key roles in development of cancer? How?

A

E6 and E7, they bind and eventually remove or inactivate two TSGs, p53 and Rb

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7
Q

How is HPV transmitted?

A

Direct contact with warts or contaminated fomites

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8
Q

How are HPV infections kept in check?

A

Innate immunity; this means most do not present with common warts and it limits the number of adolescents/adults presenting with anogenital warts

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9
Q

Is HPV perhaps the most common STD in the US?

A

You betcha

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10
Q

What is the treatment of warts? Why does recurrence happen?

A

Physical destruction of warts, but recurrence is common because the virus remains in the basal layer of skin

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11
Q

What does the subunit vaccine for HPV consist of? what has the FDA approved it for?

A

It contains the L1 capsid protein; approved as an anti-cancer vaccine

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12
Q

What type of DNA does HPV have?

A

Circular, ds-DNA genomes that are about 8 kb pairs, therefore they are on the small end of DNA virus genome complexity

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13
Q

What kind of capsid does HPV have?

A

Icosahedral

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14
Q

What is the capsid of HPV composed of?

A

Two proteins, L1 and L2 (L is for “late” because these are products of genes transcribed after DNA replication), they self-assemble to form capsids

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15
Q

Is the HPV capsid enveloped? What does this mean for the virus?

A

No, so this contributes to the stability of virus particles on skin and fomites

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16
Q

In cells permissive for HPV growth, what happens to the virus?

A

It replicates and assembles in the nucleus, released by lysing cells

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17
Q

In non-permissive cells, what happens with HPV?

A

Late gene expression does not occur and instead of virus production, infection leads to formation of transformed cells = cells capable of producing tumors

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18
Q

How is the genome of HPV maintained in benign tumor cells (warts)?

A

Extrachromosomally (similar to bacterial plasmid) in 40-50 copies

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19
Q

In malignant tumor cells (cervical carcinomas), how is HPV handled?

A

A portion of the virus genome is integrated into the host chromosome

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20
Q

What are the 5 features of transformed cells?

A

1) Immortal
2) No longer contact inhibited in cell culture
3) No longer require serum-derived growth factors
4) No longer anchorage-dependent for growth in cell culture
5) Can lead to tumor formation in syngeneic animals

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21
Q

In HPV, what do the early (E) genes encode? Which are of particular importance?

A

The proteins needed for replication and transformation; E6 and E7

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22
Q

What does E6 of HPV do?

A

Binds to TSG p53 and leads to degradation

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23
Q

What does E7 of HPV do?

A

Binds to TSG Rb and inactivates it

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24
Q

What do the combined efforts of E6 and E7 do?

A

Uncontrolled growth of the cells which leads to tumor formation

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25
Q

In malignant HPV cells, where only a portion of the virus genome is integrated into the host chromosome, what does this mean for the genes of E6 and E7?

A

The E6 and E7 genes must be intact

26
Q

Because a viral regulatory protein is disrupted when the virus genome is integrated into the host chromosome, what happens to E6 and E7 levels?

A

They are expressed at elevated levels compared to expression from the extra-chromosomally maintained copies of the genome found in benign tumor cells

27
Q

What does the elevated expression of E6 and E7 from integrated genomes is believed to be a reason for what?

A

Why the tumor cells become malignant rather than remain benign

28
Q

Where do HPVs initially infect?

A

Germinal cells in the basal layer of the skin (non permissive cells, so virus particles are not produced and the cells are transformed)

29
Q

What happens to HPV infected germinal cells?

A

They mature and migrate to the skin surface, and as they differentiate into keratinized epithelia, the cells become permissive and produce virus progeny

30
Q

What is the result of the germinal cell being infection with HPV?

A

A benign wart, due to proliferation of transformed germinal cells, which shed virus

31
Q

Why can warts return after treatment?

A

Treatment destroys the wart but does not eliminate the virus genome from the non-permissive germinal cells which serve as renewable source of infected keratinocytes

32
Q

What are the 7 diseases caused by HPV?

A

1) Common and plantar warts (verruca vulgaris)
2) Flat warts (verruca plana)
3) Anogenital warts (condyloma acuminata and condyloma plana): HPV 6 and 11
4) Sub-clinical papilloma infection (SPI): HPV 16, 18, 31
5) Cervical, penile, anal, oral, and neck cancers: HPV 16, 18, and 31
6) Infantile laryngeal papillomas: HPV 6 and 11
7) Epidermodysplasia verruciforms

33
Q

In what time frame do most warts of HPV disappear by?

A

2 years

34
Q

What are laryngeal papillomas?

A

Chronic, benign warts in the respiratory tract that generally first appear before the age of 5 (rare). Associated respiratory distress = 3% of patients die annually

35
Q

What is epidermodysplasia the result of?

A

An inherited defect in cellular immunity; they done fight off HPV infections effectively and present with numerous lesions throughout life

36
Q

Where do common and flat warts usually occur?

A

Hands or face of children or young adults

37
Q

Where do plantar warts occur?

A

Soles of the feet - can be painful and require removal

38
Q

What are penile, vulvar, or perianal warts caused by? How can they present?

A

HPV 6 and 11; can present as condyloma acuminata or condyloma plans

39
Q

Why is SPI so important?

A

Its link to cervical cancer

40
Q

How are microscopic lesions of SPI seen best?

A

Under 10x magnification after brushing the infected area with 5% acetic acid, which turns the warts white

41
Q

What does a Pap smear detect in HPV?

A

Koilocytotic (vacuolated cytoplasm) squamous epithelial cells which are indicative of HPV infection

42
Q

What % of cervical dysplasias are caused by HPV?

A

90%; but most will not lead to invasive cancer

43
Q

What warts are most prevalent in children and young adults?

A

Common and plantar

44
Q

What is the incidence of HPV in US women?

A

A wide range of 15-60% depending upon population studied and methods used to detect

45
Q

What is most commonly responsible for prominent anogenital warts?

A

HPV 6 and 11; they are very low risk for causing cervical cancer

46
Q

What fraction of sexual partners of HPV positive people will become infected?

A

About 2/3rds and few will manifest warts due to effective immune response

47
Q

What percentage of cervical cancers are HPV 16 and 18 responsible for (they lead to SPI)?

A

70%; HPV 31 is the third most likely cause

48
Q

SPI raes are 4x higher in adolescents than in women over 35, what does this suggest?

A

Most infections are eradicated; but 35 y/o and older have higher incidence of abnormal Pap smears, which suggests that persistent infections and other events lead to cervical cancers

49
Q

What are the two known cofactors in development of cervical cancer?

A

Smoking and co-infection with HSV

50
Q

How are laryngeal papillomas acquired?

A

At birth, in up to 50% of cases. HPV 6 and 11 are most common sources, risk to newborn from 1 in 100-1000 if the mother has genital warts at time of deliver

51
Q

Can HPV be grown in routine cell culture?

A

No

52
Q

How is Dx of common, plantar, and anogenital warts usually made?

A

Appearance

53
Q

For inconclusive or abnormal Pap smears, what must be done?

A

A colposcopy to look for dysplasia

54
Q

Is there an FDA approved test for detecting HPV DNA?

A

Yes

55
Q

Why is effectiveness of condoms controversial in HPV?

A

They do not cover all of the areas of skin that come in contact during intercourse (use your imagination)

56
Q

What is the FDA approved vaccine? What does it cover and what is in the vaccine?

A

Gardisil, it is quadrivalent (HPV 6, 11, 16, 18) and is a recombinant, subunit vaccine in which one of the capsid proteins (L1) is expressed in yeast and self assembles into capsid like structures

57
Q

What is Gardisil being promoted as?

A

An anticancer vaccine for females (recently males) between ages of 9-26

58
Q

When do warts usually return?

A

Immunosuppression or pregnancy

59
Q

What are the methods of removal of a wart? (6)

A

1) BCA or TCA which denatures the proteins and causes chemical destruction, surrounding tissue can burn/become irritated
2) Cryotherapy (must minimize scarring)
3) LEEP removes cells involved in cervical dysplasia
4) Podofilox is a gel, active ingredient = anti-mitotic agent (not for pregnancy)
5) Imiquimod = topical agent that stimulates localized interferon and cytokine production (not for pregnancy)
6) Intralesional interferon injection

60
Q

What has limited the number of cervical cancer deaths in the US?

A

Pap smear/early detection

61
Q

Where do cervical carcinomas continue to be a prominent, fatal cancer?

A

Developing countries; vaccine aims to spare people from this cancer

Repro Micro (6 decks)

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