GSE121651
Raw RNAseq data of HSV-1-infected mouse skin fibroblasts
Herpes simplex viruses (HSV) are responsible for a broad variety of human diseases, including cold sores, ocular herpes and herpetic encephalitis, leading to a great burden worldwide. However, the role for sex in herpes infection is controversial and unclear due to the complexity of factors involving in the formation of HSV diseases. Herein, we ask whether there is a sexual dimorphism based on the chromosomal rather than hormonal differences in the primary skin cells during low exposure of HSV. Profiling of male and female transcriptional programs reveals that cytosolic sensing pathway is induced to a greater degree in female cells, correlated with higher yields of infectious virions in male counterparts. Female skin cells distinctively reactivate Xist, a critical component of X inactivation, to silence the expression of the transcriptional repressor on X chromosome, which thereby maintains higher viperin level and further explains the different growth phenotypes between two sexes. Collectively, we propose a model that HSV-1 triggers a sex-specific regulation of antiviral response in the cytosolic sensing signaling via the control of Xist. Overall design: We report transcriptomic data from both male and female HSV-1-infected mouse skin fibroblasts to nvestigate sex differences in HSV-1 infection