Step by Step
HPV
HPV — E6 degrades p53, E7 inactivates Rb
HPV types 16 and 18 cause cervical and oropharyngeal cancers through two specific viral proteins: E6 degrades the p53 tumor suppressor, and E7 inactivates the Rb tumor suppressor. The Gardasil vaccine prevents HPV 16/18/6/11.
Example: HPV's E6 protein specifically targeting and degrading p53, removing one of the cell's key safeguards against uncontrolled division, contributing directly to cancer development.
EBV
EBV — c-myc translocation, multiple cancer types
EBV causes Burkitt's lymphoma through a c-myc translocation, along with Hodgkin's lymphoma and nasopharyngeal carcinoma.
Example: EBV-driven Burkitt's lymphoma specifically arising from a c-myc translocation that disrupts normal cell growth regulation.
HBV/HCV
HBV/HCV — chronic inflammation drives hepatocellular carcinoma
HBV and HCV cause hepatocellular carcinoma (HCC) through a different mechanism than HPV or EBV — via chronic inflammation and cirrhosis, rather than a specific oncogenic viral protein directly disabling tumor suppressors.
Example: a patient with long-standing chronic HCV infection developing cirrhosis over years, which then substantially raises their risk of eventually developing hepatocellular carcinoma.
HTLV-1/KSHV
HTLV-1 and KSHV — leukemia and Kaposi sarcoma
HTLV-1's Tax protein activates cellular proliferation, causing adult T-cell leukemia/lymphoma. KSHV (HHV-8) causes Kaposi sarcoma, particularly in AIDS patients.
Example: Kaposi sarcoma appearing in an AIDS patient with a severely weakened immune system, reflecting KSHV's opportunistic oncogenic behavior in immunocompromised hosts.
Applied Walkthrough
1
A patient with long-standing chronic hepatitis C infection develops cirrhosis and is later diagnosed with hepatocellular carcinoma.
2
Ask: does HCV cause cancer through the same mechanism as HPV (directly disabling tumor suppressor proteins)? No — HBV/HCV instead drive carcinogenesis through chronic inflammation and cirrhosis over time, a genuinely different mechanism than HPV's E6/E7 tumor suppressor disruption.
3
Contrast: if the same patient instead had cervical cancer linked to HPV 16 infection, the mechanism would specifically involve E6 degrading p53 and E7 inactivating Rb — direct molecular disruption of tumor suppressor pathways, not chronic inflammation.
4
Recognizing that different oncogenic viruses cause cancer through genuinely different mechanisms (direct tumor suppressor disruption vs. chronic inflammation vs. proliferation-activating proteins) is key to understanding this topic beyond just memorizing which virus causes which cancer.
Exam Application
Exams test whether you can match each oncogenic virus (HPV, EBV, HBV/HCV, HTLV-1, KSHV) to its associated cancer type AND its specific mechanism (tumor suppressor disruption, chromosomal translocation, chronic inflammation, or proliferation activation) — not just a simple virus-to-cancer pairing.
⚠ Common Trap
The most common trap is assuming all oncogenic viruses cause cancer through the same general mechanism. HPV directly disables tumor suppressors (E6/E7), EBV causes a specific chromosomal translocation (c-myc), HBV/HCV work through chronic inflammation and cirrhosis rather than a direct oncogenic protein, and HTLV-1's Tax protein directly activates proliferation — these are genuinely distinct mechanisms worth distinguishing.
✓ Quick Self-Check
1. What do HPV's E6 and E7 proteins do?
E6 degrades the p53 tumor suppressor; E7 inactivates the Rb tumor suppressor.
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2. What vaccine prevents HPV-related cancers, and which HPV types does it cover?
Gardasil; it prevents HPV 16, 18, 6, and 11.
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3. What genetic event does EBV cause in Burkitt's lymphoma?
A c-myc translocation.
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4. Through what mechanism do HBV and HCV cause hepatocellular carcinoma?
Chronic inflammation and cirrhosis, rather than a direct oncogenic viral protein.
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5. What cancer does KSHV (HHV-8) cause, and in what population is it particularly notable?
Kaposi sarcoma, particularly notable in AIDS patients.
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