Stacking the odds: Multiple sites for HSV-1 latency.
Shaohui WangXueying SongAlex C RajewskiChintda SantiskulvongHomayon GhiasiPublished in: Science advances (2023)
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.
Keyphrases
- induced apoptosis
- cell cycle arrest
- dendritic cells
- herpes simplex virus
- spinal cord
- endoplasmic reticulum stress
- cell death
- oxidative stress
- immune response
- type diabetes
- stem cells
- neuropathic pain
- high resolution
- genome wide
- mesenchymal stem cells
- spinal cord injury
- inflammatory response
- cell therapy
- regulatory t cells
- transcription factor
- single cell
- chemotherapy induced