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Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection

Nicholas S Heaton1, Natasha Moshkina2, Romain Fenouil3

  • 1Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029-6574, USA.

Immunity
|January 21, 2016
PubMed

Insights

Researchers identified host cell proteins essential for viral replication. Targeting Sec61-mediated translocation impaired influenza, HIV, and dengue viruses, offering a potential broad-spectrum antiviral therapy.

Area of Science:

  • Virology
  • Cellular Biology
  • Proteomics

Background:

  • Viruses are obligate intracellular parasites relying on host cell machinery for replication.
  • Understanding host-virus interactions is key to developing antiviral strategies.
  • Inhibiting host factors exploited by viruses can suppress replication and lead to pan-antiviral therapies.

Purpose of the Study:

  • To identify cellular proteins and signaling pathways crucial for influenza virus replication and infectivity.
  • To explore host factor inhibition as a potential broad-spectrum antiviral therapeutic strategy.

Main Methods:

  • Generation of fully infectious tagged influenza viruses.
  • Application of infection-based proteomics to identify host factors.
  • Utilizing mathematical modeling, genetic, and pharmacologic approaches.

Main Results:

  • Identified pivotal cellular signaling pathways required for influenza virus growth.
  • Demonstrated that modulating Sec61-mediated cotranslational translocation impairs glycoprotein proteostasis.
  • Showed selective impairment of influenza, HIV, and dengue virus replication and infectivity.

Conclusions:

  • Host factors, specifically Sec61-mediated cotranslational translocation, are critical for multiple viral infections.
  • Targeting host-virus protein-protein interactions during active replication offers a viable strategy for broad-spectrum antiviral drug development.

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