Stacking the odds: Multiple sites for HSV-1 latency.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 36696497.
- Also identified by DOI 10.1126/sciadv.adf4904 and PMC identifier 9876545.
- Licence recorded as CC BY-NC.
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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<sup>+</sup> 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.
Medical subject headings
- Herpesvirus 1, Human
- Herpes Simplex