| First Author | Sitnik KM | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 3087 |
| PubMed ID | 37248241 | Mgi Jnum | J:341010 |
| Mgi Id | MGI:7487425 | Doi | 10.1038/s41467-023-38449-x |
| Citation | Sitnik KM, et al. (2023) Fibroblasts are a site of murine cytomegalovirus lytic replication and Stat1-dependent latent persistence in vivo. Nat Commun 14(1):3087 |
| abstractText | To date, no herpesvirus has been shown to latently persist in fibroblastic cells. Here, we show that murine cytomegalovirus, a beta-herpesvirus, persists for the long term and across organs in PDGFRalpha-positive fibroblastic cells, with similar or higher genome loads than in the previously known sites of murine cytomegalovirus latency. Whereas murine cytomegalovirus gene transcription in PDGFRalpha-positive fibroblastic cells is almost completely silenced at 5 months post-infection, these cells give rise to reactivated virus ex vivo, arguing that they support latent murine cytomegalovirus infection. Notably, PDGFRalpha-positive fibroblastic cells also support productive virus replication during primary murine cytomegalovirus infection. Mechanistically, Stat1-deficiency promotes lytic infection but abolishes latent persistence of murine cytomegalovirus in PDGFRalpha-positive fibroblastic cells in vivo. In sum, fibroblastic cells have a dual role as a site of lytic murine cytomegalovirus replication and a reservoir of latent murine cytomegalovirus in vivo and STAT1 is required for murine cytomegalovirus latent persistence in vivo. |
