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Virology. 2016 Oct;497:323-327. doi: 10.1016/j.virol.2016.06.016. Epub 2016 Aug 10.

Neuronal IFN signaling is dispensable for the establishment of HSV-1 latency.

Author information

1
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA.
2
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
3
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA. Electronic address: david.a.leib@dartmouth.edu.

Abstract

IFN responses control acute HSV infection, but their role in regulating HSV latency is poorly understood. To address this we used mice lacking IFN signaling specifically in neural tissues. These mice supported a higher acute viral load in nervous tissue and delayed establishment of latency. While latent HSV-1 genome copies were equivalent, ganglia from neuronal IFN signaling-deficient mice unexpectedly supported reduced reactivation. IFNβ promoted survival of primary sensory neurons after infection with HSV-1, indicating a role for IFN signaling in sustaining neurons. We observed higher levels of latency associated transcripts (LATs) per HSV genome in mice lacking neuronal IFN signaling, consistent with a role for IFN in regulating LAT expression. These data show that neuronal IFN signaling modulates the expression of LAT and may conserve the pool of neurons available to harbor latent HSV-1 genome. The data also show that neuronal IFN signaling is dispensable for the establishment of latency.

KEYWORDS:

Herpes; Interferon; Latency; Neurons; Simplex

PMID:
27518540
PMCID:
PMC5026629
DOI:
10.1016/j.virol.2016.06.016
[Indexed for MEDLINE]
Free PMC Article

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