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Q1: What is Rous Sarcoma Virus and how does it cause cancer?
Rous Sarcoma Virus (RSV) is a retrovirus that causes cancer by introducing oncogenic genes into host cells. RSV carries the src gene, which produces proteins that disrupt normal cell growth regulation. When RSV infects cells, it integrates its genetic material into the host genome, leading to uncontrolled cell division and tumor formation.
Q2: How does RSV differ from other cancer-causing viruses?
RSV is unique as an RNA virus that directly carries an oncogene, unlike many other oncogenic viruses that disrupt normal tumor suppressor genes. This makes RSV particularly efficient at transforming cells. The presence of the src gene allows RSV to rapidly induce cellular transformation and malignant growth in infected organisms.
Q3: What role does the src gene play in RSV-induced tumorigenesis?
The src gene encodes a protein tyrosine kinase that phosphorylates cellular proteins, disrupting normal signaling pathways. This abnormal phosphorylation causes cells to lose contact inhibition and grow uncontrollably. The src protein essentially hijacks cellular machinery to promote continuous proliferation, driving viral oncogenesis.
Q4: Why is RSV significant in cancer research?
RSV was historically the first virus definitively linked to cancer, making it foundational to understanding viral oncogenesis. Studying RSV revealed how viruses introduce oncogenic genes into cells and transform normal tissue into tumors. This knowledge has shaped modern cancer research and therapeutic strategies targeting viral-induced malignancies.
Q5: How does RSV integrate into the host cell genome?
RSV, as a retrovirus, uses reverse transcriptase to convert its RNA genome into DNA, which then integrates into the host chromosome. This integration is permanent and heritable through cell division. Once integrated, the viral oncogenes are expressed continuously, maintaining the transformed phenotype in daughter cells.
Q6: What cellular changes occur when RSV transforms a normal cell?
RSV-transformed cells lose contact inhibition, grow in multiple layers, and acquire anchorage-independent growth. These cells also show altered morphology, increased motility, and resistance to apoptosis. The transformed cells develop hallmarks of malignancy, including rapid proliferation and the ability to form tumors in host organisms.
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