Paper I — 2024 June (Supplementary) (2019 Scheme) — Q4
3 min read
Paper I
2024 June (Supplementary) (2019 Scheme) · 100 marks · 180 min
Question
Oncogenic DNA viruses
Q48 marksShort Essays
Answer
Oncogenic DNA viruses can directly contribute to malignant transformation through expression of viral oncoproteins that interfere with host cell growth-regulatory pathways.
Human papillomavirus (HPV)
High-risk types (16, 18, others) express E6 and E7 oncoproteins
E6 binds and promotes degradation of p53 (tumour suppressor)
E7 binds and inactivates Rb (retinoblastoma protein), releasing E2F to drive uncontrolled cell cycle progression
Implicated in cervical carcinoma, other anogenital carcinomas, and oropharyngeal carcinoma
Hepatitis B virus (HBV)
Causes chronic hepatocyte injury and compensatory regeneration, increasing the risk of mutation accumulation
The HBx protein can also directly interfere with p53 function and activate growth-promoting signalling pathways
Viral DNA may integrate into the host genome, causing genomic instability
Implicated in hepatocellular carcinoma
Epstein-Barr virus (EBV)
Infects B lymphocytes and epithelial cells; expresses latent membrane proteins (LMP-1) that activate growth signalling pathways and inhibit apoptosis
Implicated in Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin lymphoma (subset), and post-transplant lymphoproliferative disease
Human herpesvirus-8 (HHV-8/Kaposi sarcoma herpesvirus)
Encodes viral proteins that mimic host cytokines/growth factors and inhibit apoptosis
Implicated in Kaposi sarcoma and primary effusion lymphoma, particularly in immunocompromised (HIV) patients
Common mechanistic themes
Inactivation of tumour suppressor proteins (p53, Rb)
Inhibition of apoptosis
Promotion of cell proliferation
Often require additional cofactors (immunosuppression, chronic inflammation, co-carcinogens) for full malignant transformation, reflecting the multistep nature of carcinogenesis
