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OMPR > HPV > Flashcards

HPV Flashcards

1
Q

Human Papilloma Virus (HPV)

A
  • Papillomaviridae family
  • Small, non-enveloped icosahedral DNA virus that infects skin or mucosal cells of humans.
  • Circular DNA

-High and low risk types

(Alpha HPV Genotype is the mucosal type**)

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2
Q

Types of HPV Epithelial Lesions

A

Benign: Neoplasms of squamous epithelium (warts)
Premalignant: Epithelial dysplasia
Malignant: Squamous cell carcinoma

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3
Q

Routes of Transmission

A
  • Sexual/non-sexual direct contact
  • Salivary transfer
  • Contaminated objects (fomite)
  • Autoinoculation
  • Perinatal/prenatal transmission
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4
Q

HPV Pathogenesis (general)

A
  • Incubation period is 3 weeks to 2 years
  • virus infects the basal cell and as the virus matures, it is released to the surface

VIRUS HAS TO INFECT THE BASAL KERATINOCYTES

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5
Q

HPV Pathogenesis Steps

A
  • HPV accesses and infects cells of the epithelial basal layer through breaks in the skin or mucosa
  • The virus become incorporated in the genome of the infected cell
  • The site of HPV integration into the cellular genome is in the general region of known oncogenes
  • The virus replicates during keratinocyte differentiation in the spinous and granular cell layers
  • A portion of the HPV genome encodes proteins that are capable of inducing cell proliferation and transformation
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6
Q

Molecular mechanism

A

Binding of the viral E7 protein to pRb causes release of E2F and other proteins that serve as signals for the cell cycle to progress. leading to uncontrolled cell proliferation

The HPV E6 protein ligase attaches ubiquitin molecules to p53, thereby making it inactive and subject to proteosomal degradation. Without p53, cells with changes in the DNA, such as integrated viral DNA, are not repaired. This destabilizes the cell and further increases the risk of malignant transformation.

P16 increases in cells infected with HPV!!!
P14 is also increasing and inactivating MDM which further degrades p53 and there’s no
Longer tumor suppression

P16 IS WHAT WE LOOK FOR IN HPV TESTS

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7
Q

High-risk types v. Low-risk types?

A

Persistence!!!

High-risk types clear slowly, more likely to become persistent

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8
Q

Prevalence of oral (HPV)

A 
Overall 7%
More in men 
Bimodal distribution for age 
High risk is more prevalent 
HPV-16 infection most prevalent
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9
Q

Risk Factors Associated with Prevalence

A
  • Sexual behavior
  • Male
  • Increased # of partners (vaginal or oral)
  • Tobacco smoking
  • HIV infection
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10
Q

SCCA: HPV vs tobacco and alcohol

A

HPV associated SCCa
-Wild type TP53
Low pRb
-Increased p16

Tobacco and alcohol associated SCCa

  • Mutated TP53
  • pRb overexpression
  • Decreased p16
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11
Q

Benign Oral low risk HPV lesions Clinical Appearance

A
  • Appear as single or multiple exophytic papules, either sessile and flat or pedunculated and papillary.
  • Color depends upon degree of keratinization, ranging from white to pink.
  • Size of papules generally <10mm in diameter.
  • Histologically, lesions may have koilocytes.
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12
Q

Examples of Benign Oral low risk HPV lesions

A 
Squamous papilloma
Verruca vulgaris
Condyloma acuminatum
Focal epithelial hyperplasia
Oral florid papillomatosis
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13
Q

Squamous Papilloma

A

Benign proliferation of stratified squamous epithelium resulting in a papillary, verruciform, rugose (ridged or wrinkled) mass

HPV types 6 and 11

M=F

Any age (more common in 3rd to 5th decade)

Any oral mucosal surface (palate most common)

Soft, painless, usually pedunculated, exophytic lesion with numerous fingerlike projections

Have to be removed

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14
Q

Oral Verruca Vulgaris (warts)

A
  • HPV 2, and others (1, 4, 6, 7, 11, 26, 27, 29, 41, 57, 65, 75-77)
  • Benign, HPV induced focal hyperplasia of stratified squamous epithelium
  • Contagious – transmitted by direct contact
  • Any age - Frequently seen in children
  • Anterior part of mouth more common that posterior
  • Soft, painless, usually pedunculated, exophytic lesion with numerous fingerlike projections (similar to squamous papilloma)
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15
Q

Condyloma Acuminatum (Venereal Wart)

A
  • Types 6,11
  • Virally induced proliferation of stratified squamous epithelium – usually genital or anal mucosa
  • Contagious - transmitted by direct contact
  • Incubation period – 1-3 months
  • Considered a sexually transmitted disease (if corroborated by history)

-Oral Lesions – usually anterior part of mouth
Sessile, pink, well-demarcated, non-tender exophytic mass with short, blunted surface projections

  • Tends to be larger than papilloma or verruca vulgaris
  • Characteristic clustering of multiple lesions
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16
Q

Multifocal Epithelial Hyperplasia/heck disease

A
  • Types 13, 32 and others (1, 6, 11, 16, 18, 55)
  • HPV induced localized proliferation of oral squamous epithelium
  • Endemic in some Inuit/Alaskan native and Native American communities, also seen in Puerto Rican communities
  • Crowded conditions, malnutrition
  • Usually seen in children
  • May be seen in HIV positive individuals
  • M=F
  • Histology: Focal epithelial acanthosis
17
Q

Florid Papillomatosis

A
  • HIV infection
  • Increased prevalence since advent of HAART therapy
  • Multiple HPV types
  • Down syndrome
18
Q

Histopathology-benign oral HPV lesions

A
  • Acanthosis (thickening layers)
  • Koilocytosis (virally infected cells on histo)
  • Binucleated and multinucleated keratinocytes
  • Dyskeratosis
  • Mitosoid figures
  • Basilar hyperplasia?
19
Q

Koilocytes

A
  • Pathognomonic but not required for HPV infection
  • Enlarged squamous epithelial cell with perinuclear halo around shrunken nuclei
  • Produced when a portion of the HPV genome encodes a protein that binds to and disrupts the cytoplasmic keratin network
20
Q

What percentage of oropharyngeal cancers are caused by HPV in the US?

A

70%

21
Q

What’s used to test for HPV associated cancers?

A

HPV-in-situ hybridization tests (and more recently RNA ISH) can reveal viral integration

p16 (not to be confused with HPV Type 16) immunohistochemistry is a reliable surrogate for HPV+ oropharyngeal cancer. However, it isn’t a good surrogate for HPV in oral cavity cancers (ie. a significant proportion of oral cavity cancers are p16+ yet HPV negative)

22
Q

Guidelines-HPV testing

A

Only perform testing on OROPHARYNGEAL CANCERS (16/18)

HPV testing using p16 surrogate on oropharyngeal squamous cell carcinoma
and no HPV testing on low risk HPV lesions

23
Q

Management of the Benign HPV Solitary Lesions

A

Usually appear exophytic and papillary

Excision is warranted
Consider possible recurrence

24
Q

Management of the Benign HPV Multiple Lesions

A

Use high power evacuation to prevent transmission

Treatment is controversial

Excision/ablation vs topical vs intralesional therapy (or combination)

Consider higher rate of recurrence

25
Q

Types of Excision or Ablation

A

Scalpel
Carbon dioxide laser
Electrosurgery

26
Q

Topical therapy

A

Podophyllin resin
Imiquimod (extra-oral use only)
Cidofovir
Interferon

27
Q

Topical Podophyllin

A

Topical cytotoxic agent which arrests mitosis

Genital warts and other papillomas

Not FDA approved for oral warts**

Serious adverse reaction if absorbed systemically

Pregnancy category X

28
Q

Topical Imiquimod

A

Induces cytokines and chemokines with resultant antiviral (HPV) effects

Not FDA approved for oral warts

29
Q

Intralesional therapy

A
  • Interferon alpha 2a
  • Antiviral activity of IFN’s may be related in part to an effect on dsRNA
  • Interferon enzymes may also inhibit viral penetration and uncoating, and/or viral assembly and release
  • Expression of major histocompatibility antigens by IFN’s may also contribute to antiviral activity by enhancing the lytic effects of cytotoxic T lymphocytes
30
Q

HPV Vaccination

A

2 doses are recommended for all boys and girls age 11-12 and 6 months later

Also recommended for everyone up to 26 years

Not recommended for older than 26 unless at risk for new infections (less benefit since most already exposed)

Virus like particles (VLP) of the L1 capsid protein are present in vaccine

31
Q

Oral Molluscum Contagiosum

A
  • Poxvirus
  • Presents as pink, dome-shaped, smooth-surfaced or umbilicated papules with caseous plug involving skin, lips, buccal mucosa, and palate

-Florid cases seen in immunocompromised persons
Children, young adults

-Histopathology characterized by large intracytoplasmic inclusion bodies (Henderson-Paterson bodies)

32
Q

Measles

A
  • Paramyxovirus
  • Spread through respiratory droplets
  • Runny nose, red/watery eyes, cough, fever, rash, desquamation of skin
  • Koplik’s spots, pathognomonic for measles, are discrete, bluish white punctate mucosal macules surrounded by a rim of erythema; they represent foci of epithelial necrosis
  • Often precedes skin manifestations
  • The most common location is buccal mucosa, where the lesions may resemble “grains of salt sprinkled on an erythematous background”
33
Q

Enterovirus-Coxsackie virus

A
  • Coxsackievirus infections
  • Herpangina-soft palate, red macules –> fragile vesicles
  • Hand foot and mouth disease-oral lesions more in the anterior regions (aphthous-like), hand/foot (vesicles)
  • Acute lymphonodular pharyngitis-nodules on the soft palate
  • Usually seen in children
  • Self-limiting

OMPR (8 decks)

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