Abstract
AbstractTo date, no herpesvirus has been shown to latently persist in fibroblastic cells. Here, we demonstrate that mouse CMV (MCMV), a β-herpesvirus, persists for the long term and across organs in PDGFRα+fibroblastic cells, with similar or higher genome loads than in the previously known sites of MCMV latency. Whereas MCMV gene transcription in PDGFRα+fibroblastic cells was almost completely silenced at 5 months post-infection, these cells gave rise to reactivated virusex vivo, arguing that they supported latent MCMV infection. Notably, PDGFRα+fibroblastic cells also supported productive virus replication during primary MCMV infection. Mechanistically,Stat1-deficiency resulted in increased lytic but abolished latent infection of fibroblastic cellsin vivo. In sum, fibroblastic cells have a dual role as a site of lytic MCMV replication and a reservoir of latent MCMVin vivoandStat1is critically involved in the regulation of MCMV latency.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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1. Rethinking human cytomegalovirus latency reservoir;Annals of the New York Academy of Sciences;2023-04-07