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Questions and Answers
Which HPV genotypes are responsible for approximately 70% of invasive cervical cancer cases worldwide?
What is the primary risk factor for developing cervical intraepithelial neoplasia (CIN)?
Where does HPV replicate exclusively?
What is a common clinical presentation of cutaneous warts caused by HPV?
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What role do early non-structural viral proteins E6 and E7 play in HPV infection?
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What types of warts are primarily caused by HPV 6 and 11?
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How does HPV evade immune recognition in the epithelium?
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What happens to the majority of HPV infections within 12–24 months?
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Which of the following viruses is classified as a DNA tumor virus?
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What characterizes oncogenic viruses?
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Which proteins are associated with tumor-suppressor genes?
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Which HPV type is most commonly linked to cervical cancer?
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What is the primary mode of transmission for high-risk HPV types?
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Which of the following cell types gives rise to carcinoma?
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What term describes the process normal cells undergo to become malignant?
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What best describes the role of proto-oncogenes?
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Which term refers to the continuous proliferation of a clone of cells in cancer?
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What percentage of human cancers worldwide are estimated to have a viral etiology?
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Which area is most commonly affected by lesions associated with HPV infections?
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What is the most common cause of laryngeal papillomatosis?
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Which statement is true regarding epidermodysplasia verruciformis?
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How does HPV oncogenesis begin?
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Which factor increases the risk of HPV persistence and cervical cancer?
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What is an effective prevention method for cervical cancer?
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What is the treatment focus for infants affected by laryngeal papillomatosis?
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What condition does a CD4 cell count of < 200 indicate in relation to HPV?
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What is the recommended age for females to receive the Cervarix vaccine?
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Which HPV vaccine targets serotypes 6, 11, 16, and 18?
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Study Notes
HPV and Cervical Cancer
- Human Papillomavirus (HPV) is a non-enveloped, double-stranded DNA virus with over 200 types.
- HPV is sexually transmitted and can also be transmitted in utero or perinatally.
- About 15 HPV types are linked to cancer.
- High-risk (hr) types are associated with malignancy, particularly HPV 16 and 18.
- Low-risk types are associated with warts.
- hrHPV 16 and 18 are responsible for ~90% of anal cancers, ~70% of all cervical cancer cases and oropharyngeal tumors, and ~40% of penile, vulvar, and vaginal cancers.
- hrHPV 31, 33, 45, 52, and 58 also contribute to cancers, but to a lesser extent.
HPV Replication
- HPV replicates exclusively in stratified squamous epithelium, requiring differentiating epithelium for a complete cycle.
- HPV enters basal epithelial cells through micro-abrasions.
- Early non-structural viral proteins (E6 and E7) are expressed in the basal layer.
- These proteins stimulate infected cells to proliferate faster and replicate the viral genome.
- As epithelial cells mature and move up the epithelial layer, the virus's structural genes (L1 and L2) are expressed.
- Structural viral proteins are produced, new virus particles assemble, and the virus is shed as infected cells desquamate.
- Epithelium is an immune-privileged site, allowing the virus to evade immune recognition and persist for months or years.
HPV and Oncogenesis
- HPV DNA can integrate into host chromosomes.
- Viral proteins (E6 and E7) interfere with cell cycle control.
- E6 binds to p53, a tumor suppressor gene, and E7 binds to pRb, another tumor suppressor.
- The integration of HPV DNA can activate c-myc, leading to uncontrolled cell growth.
HPV and STIs
- HIV infection is associated with increased HPV persistence and the development of cervical intraepithelial lesions (CIN).
- HIV-infected females with a CD4 cell count below 200 have a seven-fold increased incidence of cervical cancer.
- Antiretroviral therapy (ART) can reduce HPV persistence and allow for clearance of the virus.
- HSV 1 and 2 infection allows for better access to the basal cell layer, potentially leading to increased persistence and oncogenic activity of HPV.
HPV and Cervical Cancer
- Most HPV infections are transient and become undetectable in 12-24 months.
- Persistent HPV infection with an oncogenic type is a major risk factor for CIN progression to cancer.
Clinical Spectrum of HPV Infection
- Most HPV infections are clinically silent.
- A small minority of individuals develop clinically apparent lesions, such as warts.
- Cutaneous warts are caused by HPV types 1, 2, 3, 4, 5, and 8.
- Mucosal warts are mainly caused by HPV types 6 and 11.
- Laryngeal papillomatosis (warts in the larynx) is commonly seen in infants and young children, usually acquired during passage through the birth canal.
- Epidermodysplasia verruciformis is a rare condition caused by mutations in the EVER1 or EVER2 genes, leading to a defect in cell-mediated immunity and high HPV susceptibility.
Prevention of Cervical Cancer
- Vaccination: Cervarix (serotypes 6 and 11) and Gardasil 4 (serotypes 6, 11, 16, and 18).
- Behavior change: Limiting high-risk exposure.
- Treatment of HIV and other STIs.
- Cervical cytology screening: Reduces the incidence of cervical cancer by 70%.
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Description
This quiz covers the essential aspects of Human Papillomavirus (HPV) and its association with cervical cancer. It discusses the types of HPV, their transmission, and the implications of high-risk strains in cancer development. Understand the replication process of HPV and its impact on epithelial cells.
