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Cellular entry of polyomaviruses

Billy Tsai1, Mengding Qian

  • 1Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA. btsai@umich.edu

Current Topics in Microbiology and Immunology
|April 8, 2010
PubMed

Insights

Polyomaviruses (Pys) hijack host cells through a multi-step entry process. These viruses utilize cellular machinery similar to bacterial toxins to deliver their DNA genome to the nucleus for replication.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Polyomaviruses (Pys) are nonenveloped DNA tumor viruses with significant medical relevance, including human pathogens like BK and JC viruses.
  • Effective Py infection requires navigating host cell entry pathways, involving intracellular transport and conformational changes for genome delivery.
  • Understanding Py entry mechanisms is crucial for developing antiviral strategies and comprehending viral pathogenesis.

Purpose of the Study:

  • To provide a comprehensive review of the current understanding of Polyomavirus entry mechanisms into host cells.
  • To elucidate the sequential steps involved in Py transport from the plasma membrane to the nucleus.
  • To highlight the parallels between Py entry and the intoxication pathways of AB(5) bacterial toxins.

Main Methods:

  • Review of existing scientific literature on Polyomavirus entry, intracellular trafficking, and host-pathogen interactions.
  • Comparative analysis of Polyomavirus and bacterial toxin entry mechanisms.
  • Synthesis of data from various studies to present a coherent model of Py cellular entry.

Main Results:

  • Polyomaviruses engage specific host cell receptors to initiate entry.
  • Pys are trafficked to the endoplasmic reticulum (ER) and subsequently cross the ER membrane.
  • Key steps in Py entry, including receptor engagement, ER targeting, membrane penetration, and nuclear entry, share similarities with AB(5) bacterial toxin intoxication pathways.

Conclusions:

  • Polyomavirus entry is a complex, multi-step process involving hijacking of host cell machinery.
  • The striking resemblance to bacterial toxin entry suggests conserved cellular mechanisms for pathogen translocation.
  • This conserved pathway provides a general principle guiding the entry of both Polyomaviruses and bacterial toxins into host cells.

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