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Host Src controls gallid alpha herpesvirus 1 intercellular spread in a cellular fatty acid metabolism-dependent

Zhitao Wang1, Bangyao Sun2, Qi Gao3

  • 1Division of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin, 150069, People's Republic of China; College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.

Virology
|August 20, 2019
PubMed

Insights

Proto-oncogene tyrosine-protein kinase Src (Src) regulates gallid alpha herpesvirus 1 (ILTV) spread. Inhibiting Src accelerates ILTV spread via fatty acid metabolism, impacting viral cytopathic effects.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Gallid alpha herpesvirus 1 (ILTV) spread mechanisms are not fully understood.
  • Proto-oncogene tyrosine-protein kinase Src (Src) is a key host factor in ILTV infection.

Purpose of the Study:

  • To elucidate the role of Src in ILTV intercellular spread.
  • To identify molecular pathways modulated by Src during ILTV infection.

Main Methods:

  • Inhibition of Src kinase activity in infected cells.
  • Analysis of viral replication, cell proliferation, and viral spread.
  • Assessment of extracellular vesicles and cell-to-cell connections.
  • Genome-wide transcriptional profiling and functional validation.

Main Results:

  • Src inhibition significantly accelerated ILTV spread, independent of viral replication or cell proliferation.
  • Enhanced spread was not mediated by neutralizing antibodies, extracellular vesicles, or direct cell-to-cell connections.
  • Fatty acid metabolism was identified as a critical pathway regulated by Src, influencing ILTV intercellular spread and cytopathic effect.

Conclusions:

  • Src controls ILTV cell-to-cell spread through a mechanism dependent on cellular fatty acid metabolism.
  • Modulation of fatty acid metabolism by Src impacts ILTV's cytopathic effect.
  • Targeting Src or related metabolic pathways may offer novel antiviral strategies against ILTV.
Keywords:
AlphaherpesvirusFatty acid metabolismSrcViral spreadVirus-host interactions

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