Postinfection Metabolic Reprogramming of the Murine Trigeminal Ganglion Limits Herpes Simplex Virus-1 Replication
Chandrashekhar D. Patil, Rahul K. Suryawanshi, Divya Kapoor, Deepak Shukla
Abstract
The more severe ocular pathologies associated with HSV-1 infection are significant vision loss, ocular morbidity, and herpetic keratitis. The current clinical landscape lacks curative drugs and vaccines against HSV-1, a heavy burden associated with this neurotropic, ubiquitous pathogen. The virus is notoriously successful in establishing latency in the host TG, where it remains dormant with periodic reactivations in response to various stimuli like stress and immunosuppression. Metabolic perturbations in tissue microenvironment likely aid the virus in establishing its latent state along with subsequent reactivations yet remain poorly characterized. Here, we used mass spectrometry coupled with statistical data analysis to study the host metabolome in the TG during HSV-1 infection and identify metabolites that likely regulate infection.