Stacking the odds: Multiple sites for HSV-1 latency

Author:

Wang Shaohui1ORCID,Song Xueying2,Rajewski Alex2ORCID,Santiskulvong Chintda2,Ghiasi Homayon1ORCID

Affiliation:

1. Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

2. Applied Genomics, Computation, and Translational Core, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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