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Host proteostasis modulates influenza evolution.

Angela M Phillips1, Luna O Gonzalez2, Emmanuel E Nekongo1

  • 1Department of Chemistry, Massachusetts Institute of Technology, Cambridge, United States.

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Summary
This summary is machine-generated.

Host cell proteostasis influences RNA virus evolution by shaping accessible mutations and selection pressures. Understanding these host-pathogen interactions can guide the development of novel antiviral therapies.

Keywords:
Hsp90biochemistryevolutionary biologygenomicsheat shock factor 1heat shock responsemutational landscapenoneselection

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Area of Science:

  • Virology
  • Molecular Biology
  • Host-Pathogen Interactions

Background:

  • RNA viruses evolve rapidly due to high mutation rates, producing protein variants that challenge folding and function.
  • Viral evolution is constrained by the biophysical limitations of these protein variants.
  • Host proteostasis, the maintenance of protein homeostasis, may critically influence viral fitness and evolution.

Purpose of the Study:

  • To investigate the role of host proteostasis in shaping RNA virus evolution.
  • To determine if host proteostasis environments impact the selection and accessibility of viral mutations.

Main Methods:

  • Propagating influenza virus in host cells with chemically modulated proteostasis levels.
  • Analyzing the influenza genome to assess selection pressures and mutational trajectories under different proteostasis conditions.

Main Results:

  • Host proteostasis significantly impacts the nature of selection acting on the influenza genome.
  • The accessibility of specific evolutionary pathways for the virus is demonstrably affected by host proteostasis.
  • Divergent proteostasis environments led to distinct patterns of viral genome evolution.

Conclusions:

  • Host proteostasis is a critical factor constraining and directing RNA virus evolution.
  • These findings offer insights into host-pathogen dynamics and the potential for proteostasis-targeted antivirals.
  • Developing resistance-refractory antiviral strategies may involve modulating host cell proteostasis mechanisms.