EGR proteins mediate interferon-independent anti-HSV-1 responses through viral and host targets

Herpes simplex virus type I (HSV-1) establishes a latent infection that evades the host's defense system, and the latent virus can be reactivated by some stimulation. At present,a key problem in the latent studies of HSV-1 has not been clarified, that is, HSV-1 mainly selectively latent in neurons. Therefore, we have found the host transcription factor EGR in Neuro-2a cells by RNA-seq. EGR1 regulates HSV-1 replication and latency by binding to the viral genome or recruiting co-factors. Our data intend to find the role and mechanism of EGR family repressing HSV-1 replication and promoting HSV-1 latency. This study will provide a theoretical basis for the development of drugs to treat of HSV-1 infection. Overall design: Neuro-2a cells( knockout EGR1) were cultured in 100-mm plates for 24 h and then infected with KOS virus strain for 5 h before being harvested for chip-seq. Library preparation and sequencing were performed by Novogene.