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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
11:28

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Published on: October 7, 2011

Host factors and measles virus replication

Sebastien Delpeut1, Ryan S Noyce, Ricky W C Siu

  • 1Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada.

Current Opinion in Virology
|November 14, 2012
PubMed

Insights

Measles virus (MeV) uses host cell factors like SLAM/CD150 and nectin-4 for entry and replication. It also employs strategies to evade the host

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Measles virus (MeV) infection relies on specific host cell factors for its lifecycle.
  • Understanding these interactions is crucial for comprehending MeV pathogenesis and developing interventions.

Purpose of the Study:

  • To provide a general overview of host cell factors facilitating MeV infection and replication.
  • To highlight the roles of specific viral entry receptors and intracellular factors.
  • To describe MeV strategies for evading host innate immunity.

Main Methods:

  • Review of current scientific literature on measles virus-host interactions.
  • Emphasis on studies detailing viral entry mechanisms and intracellular processes.
  • Discussion of findings from proteomic studies and genome-wide RNAi screens.

Main Results:

  • Identified key host cell surface receptors, including SLAM/CD150 (lymphocyte) and PVRL4/nectin-4 (epithelial).
  • Discussed intracellular host factors (HSP72, Prdx1, tubulin, casein kinase, actin) involved in viral RNA synthesis and assembly.
  • Outlined MeV strategies to overcome innate immune responses, particularly interferon.

Conclusions:

  • Host cell factors are indispensable for measles virus entry, replication, and pathogenesis.
  • Specific receptors and intracellular proteins play critical roles in the MeV lifecycle.
  • MeV actively counteracts host antiviral defenses, necessitating further research into these mechanisms.

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