PDGFRα+ fibroblasts are a major site of cytomegalovirus replication in vivo and genome maintenance during latency
Sitnik, K. M.; Krstanovic, F.; Goedecke, N.; Rand, U.; Kubsch, T.; Maas, H.; Kim, Y.; Brizic, I.; Cicin-Sain, L.
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To date, no herpesvirus has been shown to latently persist in fibroblastic cells. Here, we demonstrate that mouse CMV (MCMV), a {beta}-herpesvirus, persists for the long term and across organs in PDGFR+ fibroblastic cells, with similar or higher genome loads than in the previously known sites of MCMV latency. Whereas MCMV gene transcription in PDGFR+ fibroblastic cells was almost completely silenced at 5 months post-infection, these cells gave rise to reactivated virus ex vivo, arguing that they supported latent MCMV infection. Notably, PDGFR+ fibroblastic cells also supported productive virus replication during primary MCMV infection. Mechanistically, Stat1-deficiency resulted in increased lytic but abolished latent infection of fibroblastic cells in vivo. In sum, fibroblastic cells have a dual role as a site of lytic MCMV replication and a reservoir of latent MCMV in vivo and Stat1 is critically involved in the regulation of MCMV latency.
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