Postinfection Metabolic Reprogramming of the Murine Trigeminal Ganglion Limits Herpes Simplex Virus-1 Replication

Chandrashekhar D. Patil, Rahul K. Suryawanshi, Divya Kapoor, Deepak Shukla

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Herpes simplex virus type-1 (HSV-1) infections are known to alter the host metabolism for efficient propagation in vitro. However, in vivo metabolic perturbations upon prolonged HSV-1 infection remain poorly understood. We used high-resolution liquid chromatography coupled with mass spectrometry (LC-MS) and functional assays to determine the state of the trigeminal ganglion (TG) tissue metabolism upon prolonged corneal HSV-1 infection in a murine model. The metabolomics data indicated significant alterations in the host metabolic profile. After HSV-1 infection, the TG microenvironment assumed downregulation of central carbon metabolism and nucleotide synthesis pathways. We validated our observations using in vitro and ex vivo models through targeted inhibition of crucial metabolic polyamine pathways identified in our metabolomics screen. Our findings collectively suggested that HSV-1 infection altered the host metabolic product regulations that limit the energy and macromolecular precursors required for viral replication.

Original languageEnglish
JournalmBio
Volume13
Issue number5
DOIs
StatePublished - 1 Sep 2022
Externally publishedYes

Keywords

  • herpesvirus
  • latency
  • metabolomics
  • polyamines
  • trigeminal ganglion

ASJC Scopus subject areas

  • Microbiology
  • Virology

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