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Related Experiment Video

Updated: May 16, 2026

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

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

Summary

This summary is machine-generated.

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

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Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses

Published on: April 4, 2019

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.