Fibroblasts are a site of murine cytomegalovirus lytic replication and Stat1-dependent latent persistence in vivo

Katarzyna M. Sitnik (), Fran Krstanović, Natascha Gödecke, Ulfert Rand, Tobias Kubsch, Henrike Maaß, Yeonsu Kim, Ilija Brizić and Luka Čičin-Šain ()
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Katarzyna M. Sitnik: Helmholtz Centre for Infection Research
Fran Krstanović: University of Rijeka
Natascha Gödecke: Helmholtz Centre for Infection Research
Ulfert Rand: Helmholtz Centre for Infection Research
Tobias Kubsch: Helmholtz Centre for Infection Research
Henrike Maaß: Helmholtz Centre for Infection Research
Yeonsu Kim: Helmholtz Centre for Infection Research
Ilija Brizić: University of Rijeka
Luka Čičin-Šain: Helmholtz Centre for Infection Research

Nature Communications, 2023, vol. 14, issue 1, 1-13

Abstract: Abstract To date, no herpesvirus has been shown to latently persist in fibroblastic cells. Here, we show that murine cytomegalovirus, a β-herpesvirus, persists for the long term and across organs in PDGFRα-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 PDGFRα-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, PDGFRα-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 PDGFRα-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.

Date: 2023
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DOI: 10.1038/s41467-023-38449-x

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