In this study, mitochondria migrated to a perinuclear region in the cytopla
sm in herpes simplex virus (HSV)-infected cells. HSV infection did not prom
ote the expression of cytochrome c oxidase subunit 2 but did promote that o
f stress-responsive HSP60, both of which are known to be components of mito
chondria, The levels of cellular ATP and lactate and mitochondrial membrane
potential were maintained for at least 6 h but decreased at the late stage
of infection. It was also found that the UL41 and UL46 gene products, both
of which are known to be tegument proteins, accumulated in the perinuclear
region. The clustering of mitochondria and the accumulation of tegument pr
oteins were completely blocked by the addition of nocodazole and vinblastin
e. These results suggest that mitochondria respond to the stimulation of HS
V infection, migrating with tegument proteins along microtubules to a site
around the nucleus, and maintain function until at least the middle stage o
f infection.