Oncogenic Viruses - Tiny Tumour Triggers
- Definition: Viruses causing cancer by disrupting host cell cycle control and growth regulation.
- Classification:
- DNA Viruses: e.g., HPV, EBV, HBV, HHV-8, MCPyV.
- RNA Viruses: e.g., HTLV-1, HCV.
- General Mechanisms:
- Direct: Viral oncogenes (v-onc) integrate or persist episomally. Key actions: activate proto-oncogenes, inactivate tumour suppressor genes (TSGs) like p53, Rb. Results in cell transformation, immortalization.
- Indirect: Chronic inflammation (e.g., HBV, HCV leading to hepatocellular carcinoma) or immunosuppression.
- Key Terms: Proto-oncogenes, TSGs (p53, Rb), transformation, immortalization, latency (viral persistence).
⭐ HPV E6 oncoprotein targets p53 for ubiquitin-mediated degradation; E7 oncoprotein binds and inactivates Rb.
DNA Oncogenic Viruses - Genome Invaders
These viruses integrate their genetic material or viral proteins to disrupt host cell cycle regulation, leading to uncontrolled proliferation.
- Key Mechanisms:
- Inactivation of tumor suppressor proteins (p53, Rb)
- Activation of proto-oncogenes
- Chronic inflammation leading to cell damage and regeneration
| Virus | Family | Key Proteins/Genes | Target Pathways/Mechanism | Associated Cancers |
|---|---|---|---|---|
| HPV | Papillomaviridae | E6, E7 | E6 → p53 degradation; E7 → Rb inactivation | Cervical, anogenital, oropharyngeal carcinomas 📌 16, 18 >70% cervical Ca |
| EBV | Herpesviridae | LMP1, EBNA2 | LMP1 (CD40 mimic), EBNA2 (gene activation) | Burkitt's & Hodgkin's lymphoma, Nasopharyngeal Ca, Gastric Ca |
| HBV | Hepadnaviridae | HBx | HBx → cell cycle disruption, p53 inactivation (indirect) | Hepatocellular carcinoma (HCC) |
| HHV-8 (KSHV) | Herpesviridae | LANA, v-cyclin, v-FLIP | Proliferation ↑, Apoptosis ↓ | Kaposi's sarcoma, Primary effusion lymphoma |
| MCV | Polyomaviridae | LT & sT antigens | LT → p53 & Rb inactivation | Merkel cell carcinoma |
RNA Oncogenic Viruses - Reverse Rebels
RNA viruses with oncogenic potential, primarily HTLV-1 (a retrovirus) and HCV (a Flavivirus). They employ distinct mechanisms for carcinogenesis.
- Human T-cell Lymphotropic Virus 1 (HTLV-1)
- Retrovirus; integrates into host genome.
- Key protein: Tax (transcriptional activator/co-activator).
- Mechanism: Tax transactivates cellular genes (e.g., IL-2, IL-2R), promotes cell proliferation, induces genomic instability, inhibits apoptosis.
- Cancer: Adult T-cell Leukemia/Lymphoma (ATLL).
- Hepatitis C Virus (HCV)
- Flavivirus; RNA virus, does not integrate into host DNA.
- Key proteins: Core, NS3, NS5A.
- Mechanism: Chronic inflammation & regeneration → cirrhosis; oxidative stress → DNA damage; viral proteins directly alter cell signaling pathways (e.g., interfere with p53).
- Cancer: Hepatocellular Carcinoma (HCC).
| Virus | Family | Key Proteins | Mechanism | Associated Cancers |
|---|---|---|---|---|
| HTLV-1 | Retroviridae | Tax | Transactivation of cellular genes, genomic instability, anti-apoptosis | ATLL |
| HCV | Flaviviridae | Core, NS3, NS5A | Chronic inflammation, oxidative stress, direct protein effects on signaling | HCC |
📌 RNA Rebels: HTLV-1 Tax Activates T-cells; HCV Causes Hepatocellular Carcinoma via Chronic inflammation.
High‑Yield Points - ⚡ Biggest Takeaways
- HPV types 16, 18 are key for cervical cancer; E6 targets p53, E7 targets Rb.
- EBV is associated with Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's lymphoma.
- HBV & HCV significantly increase risk for hepatocellular carcinoma (HCC).
- HTLV-1 is the causative agent for Adult T-cell Leukemia/Lymphoma (ATLL).
- KSHV/HHV-8 causes Kaposi's sarcoma and primary effusion lymphoma.
- Key mechanisms: inactivating tumor suppressors (p53, Rb), activating oncogenes, viral integration, chronic inflammation.
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