Stacking the odds: Multiple sites for HSV-1 latency

Sci Adv. 2023 Jan 25;9(4):eadf4904. doi: 10.1126/sciadv.adf4904. Epub 2023 Jan 25.

Abstract

A hallmark of herpes simplex virus (HSV) infection is the establishment of latent virus in peripheral sensory ganglia of the latently infected host. We and others originally reported that the latency-associated transcript (LAT) is the only abundantly expressed viral gene in neurons within trigeminal ganglia (TG) of a latently infected host. Here, we investigated the possible contribution of various cells [i.e., B cells, dendritic cells (DCs), fibroblasts, glial cells, innate lymphoid cells (ILCs), macrophages, microglia, monocytes, natural killer cells, neurons, neutrophils, and T cells] isolated from TG of latently infected mice. Our results demonstrated that all of these cell types contain LAT, with DCs, neurons, and ILCs having the most LAT+ cells. These results suggest that HSV-1 can establish a quiescent/latent infection in a subset of nonneuronal cells, which enhances the chances that the virus will survive in its host.

MeSH terms

  • Animals
  • Herpes Simplex*
  • Herpesvirus 1, Human* / physiology
  • Immunity, Innate
  • Lymphocytes / metabolism
  • Mice
  • Virus Latency