Difficulty: Easy
Correct Answer: All of these
Explanation:
Introduction:
Some human viruses possess oncogenic properties, meaning they can drive cellular transformation, immortalization, or dysregulated proliferation either in experimental systems or within the human host. This question examines recognition of three classic oncogenic viruses—HBV, HTLV-1, and EBV—that are well documented to transform infected cells and contribute to cancer pathogenesis.
Given Data / Assumptions:
Concept / Approach:
Cellular transformation by viruses typically involves viral proteins that alter host cell cycle regulation, apoptosis, or genomic stability. For HBV, the HBx protein and chronic inflammatory microenvironment are key. HTLV-1 uses Tax and HBZ to dysregulate signaling and proliferation in T cells. EBV employs latent proteins (e.g., LMP1, EBNA2) to drive B-cell activation and survival. If each listed virus has credible evidence of transformation/oncogenicity, then a combined option is correct.
Step-by-Step Solution:
Step 1: Evaluate HBV: chronic infection and HBx contribute to oncogenesis in the liver.Step 2: Evaluate HTLV-1: Tax/HBZ promote T-cell proliferation leading to adult T-cell leukemia/lymphoma.Step 3: Evaluate EBV: latent genes transform B cells; multiple EBV-associated cancers are documented.Step 4: Integrate: all three are transforming/oncogenic; therefore select the comprehensive option.
Verification / Alternative check:
Oncovirology references consistently list HBV, HTLV-1, and EBV among definitive human oncogenic viruses, with mechanistic and epidemiological support. Multiple in vitro systems also show immortalization/transformation of target cells by these agents under defined conditions.
Why Other Options Are Wrong:
Common Pitfalls:
Confusing “transforming in vitro” with “causing cancer” in vivo; both are relevant but not identical. Another pitfall is assuming only DNA tumor viruses transform; HTLV-1 is an RNA retrovirus with clear oncogenicity.
Final Answer:
All of these.
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