Lecture 7: Virology (HPV Focus) Flashcards
What type of virus is HPV, and what is its genome structure?
HPV is a non-enveloped, icosahedral double-stranded DNA virus (~8kbp). It infects squamous epithelial cells and has 200+ genotypes, with ~40 sexually transmitted.
Compare high-risk and low-risk HPV types.
High-risk (e.g., HPV-16/18): Cause cancers (cervical, anal).
Low-risk (e.g., HPV-6/11): Cause benign warts (genital, laryngeal).
Describe key steps in HPV infection.
Attachment: Binds basement membrane via heparin sulfate proteoglycans (HSPGs).
Entry: Endocytosis → uncoating in endosomes → nuclear entry during mitosis.
Replication: E6/E7 oncoproteins drive cell cycle; virions assemble in nucleus.
Release: Shed with dead keratinocytes.
How do E6 and E7 promote cancer?
E6: Degrades p53 (apoptosis blocker).
E7: Binds pRb, releasing E2F to push cell cycle → uncontrolled proliferation.
How does HPV evade the immune system?
Low early protein expression.
Capsid proteins shed quickly from epithelium.
E6/E7 inhibit antigen presentation.
Match HPV types to diseases:
HPV-1/2/4: Plantar warts.
HPV-6/11: Genital/laryngeal warts.
HPV-16/18: Cervical cancer (70% of cases).
How is HPV diagnosed?
Pap smear: Identifies koilocytes (abnormal cells).
PCR/DNA probes: Detect HPV DNA (e.g., HPV-16/18).
Acetic acid test: Turns infected areas white.
Compare HPV vaccines.
Gardasil-9: Protects against 9 types (6/11/16/18/31/33/45/52/58).
Cervarix (discontinued): Targeted HPV-16/18.
Best efficacy: Pre-sexual activity (ages 9–13).
Why does HPV cause cervical cancer?
Viral DNA integrates into host genome → E6/E7 overexpression → p53/pRb inactivation → genomic instability → carcinoma.
How are HPV-related warts/cancers treated?
Warts: Imiquimod (immune booster), cryotherapy, surgery.
Cancer: Surgical removal (e.g., LEEP for cervical lesions).
