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

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.

journal_name

Virology

journal_title

Virology

authors

Rosato PC,Katzenell S,Pesola JM,North B,Coen DM,Leib DA

doi

10.1016/j.virol.2016.06.016

subject

Has Abstract

pub_date

2016-10-01 00:00:00

pages

323-327

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(16)30157-X

journal_volume

497

pub_type

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