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Viruses target mitochondria to promote viral replication, and infection-induced stress during the progression of infection leads to the regulation of antiviral defenses and mitochondrial metabolism which are opposed by counteracting viral factors. The precise structural and functional changes that underlie how mitochondria react to the infection remain largely unclear. Here we show that as herpes simplex virus type 1 lytic infection proceeds from early to late stage of infection, the expression of mitochondrial protein-encoding host genes involved in the respiratory chain, apoptosis, and structural organization of mitochondria is extensively regulated. High-resolution microscopy and interaction analyses unveiled infection-induced emergence of rough and elongated mitochondria relocalized at the nuclear periphery, a significant increase in the number and clustering of ER-mitochondria contact sites, and thickening and …