The c-Rel transcription factor limits early interferon and neuroinflammatory responses to prevent herpes simplex encephalitis onset in mice.

ABSTRACT: Herpes simplex virus type 1 (HSV-1) is the predominant cause of herpes simplex encephalitis (HSE), a condition characterized by acute inflammation and viral replication in the brain. Host genetics contribute to HSE onset, including monogenic defects in type I interferon signaling in cases of childhood HSE. Mouse models suggest a further contribution of immune cell-mediated inflammation to HSE pathogenesis. We have previously described a truncating mutation in the c-Rel transcription factor (Rel^C307X) that drives lethal HSE in 60% of HSV-1-infected Rel^C307X mice. In this study, we combined dual host-virus RNA sequencing with flow cytometry to explore cell populations and mechanisms involved in Rel^C307X-driven HSE. At day 5 postinfection, prior to HSE clinica

SUBMITTER: Mancini M 

PROVIDER: S-EPMC8551191 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature