Oncogene theory: What does it explain in the context of virus–host interactions and cancer biology?

Introduction:
The oncogene theory underpins modern tumor virology and molecular oncology. It addresses how viral elements or dysregulated cellular genes can drive uncontrolled proliferation, loss of growth control, and malignant phenotypes. Understanding this theory clarifies viral carcinogenesis (e.g., retroviruses, DNA tumor viruses) and even non-viral oncogene activation.

Given Data / Assumptions:

• The question asks for the core idea of the oncogene theory.
• Oncogenes can be viral (v-onc) or cellular (proto-oncogenes that become activated oncogenes).
• Transformation refers to conversion of normal cells into tumor cells.

Concept / Approach:
Oncogene theory proposes that certain genes, when introduced by viruses or aberrantly activated within host cells, can induce transformation. Retroviruses may carry v-onc genes or activate host proto-oncogenes via insertional mutagenesis. DNA tumor viruses can disrupt cell-cycle regulators (e.g., p53, Rb) using viral oncoproteins, tipping the balance toward proliferation and away from apoptosis.

Step-by-Step Solution:
Identify the focus: transformation of normal cells. Relate viral mechanisms: v-onc carriage, promoter insertion, enhancer activation, or disruption of tumor suppressors. Conclude that the theory explains viral induction of tumors.

Verification / Alternative check:
Classical examples include Rous sarcoma virus (v-src), human papillomavirus (E6/E7 impacting p53/Rb), and HBV/HTLV mechanisms influencing oncogenesis.

Why Other Options Are Wrong:

• Chemical inactivation: Disinfection, not oncogenesis.
• Viral replication: General virology, not transformation-specific.
• None of these / RT inhibition: Do not address tumor formation.

Common Pitfalls:
Equating transformation with mere infection; oncogenesis involves stable genetic or regulatory changes leading to unregulated growth.

Final Answer:
The oncogene theory explains how viruses transform normal cells into tumor cells.