Hamster polyomavirus

From WikiMD's Food, Medicine & Wellness Encyclopedia

Hamster Polyomavirus (HaPV) is a virus belonging to the Polyomaviridae family, which is known to cause cancerous growths in hamsters. This virus is an important model for studying viral oncogenesis, the process by which viruses cause cancer in their hosts. The study of HaPV has contributed significantly to our understanding of the molecular mechanisms underlying tumor formation and the role of viruses in this process.

Overview[edit | edit source]

Hamster Polyomavirus was first identified in the early 1960s when it was discovered that it could induce skin tumors and sarcomas in newborn hamsters. Unlike many other polyomaviruses, HaPV is highly oncogenic, meaning it has a high capacity to cause cancer. The virus is small, with a circular double-stranded DNA genome enclosed in a protein capsid. HaPV infects cells and integrates its DNA into the host cell's genome, disrupting normal cell function and leading to tumor development.

Life Cycle[edit | edit source]

The life cycle of HaPV begins with the virus binding to the surface of a susceptible host cell. After entry into the cell, the viral DNA is transported to the nucleus, where it can either remain episomal or integrate into the host genome. In the nucleus, the viral DNA is transcribed and replicated using the host's cellular machinery. The newly synthesized viral genomes are then packaged into capsids, and mature virions are released from the cell to infect new cells. This life cycle is typical of polyomaviruses and is crucial for understanding how HaPV causes disease.

Pathogenesis[edit | edit source]

The pathogenesis of HaPV-related tumors involves several key steps. After integration of the viral DNA into the host genome, the expression of viral oncogenes can lead to uncontrolled cell proliferation and tumor formation. HaPV encodes for early proteins, such as large T-antigen, which are directly involved in the transformation of infected cells. These viral proteins can interfere with tumor suppressor proteins like p53 and Rb, leading to cell cycle deregulation and oncogenesis.

Research and Implications[edit | edit source]

Research on HaPV has provided valuable insights into the mechanisms of viral oncogenesis. Studies have shown how viral proteins interact with host cell pathways to promote tumor development, offering potential targets for therapeutic intervention. Furthermore, understanding the life cycle and pathogenesis of HaPV has implications for the development of antiviral strategies and cancer prevention.

See Also[edit | edit source]

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Contributors: Prab R. Tumpati, MD