Herpesvirus remodel organization and function of mitochondria as infection proceeds
During the infection, viruses target mitochondria to promote viral replication. Infection-induced stress during the progression of infection leads to the regulation of antiviral defenses and mitochondrial metabolism which are opposed by counteractions of viral factors. The precise structural and functional changes that underlie how mitochondria react to the infection remain largely unclear. Our multimodal integration of advanced imaging, genomics, and metabolomics draws a comprehensive picture of time-dependent changes in mitochondria as HSV-1 infection proceeds from early to late infection. Overall design: Vero cells were infected with HSV1 and samples for GRO-Seq were collected 4 or 8 hours post infection.