Abstract
Herpes simplex virus type 2 (HSV-2) is the causative agent of genital herpes. Matsuzawa etal have demonstrated that, in a mouse model, HSV-2 pathology is influenced by the time infection occurs. Increased expression of the HSV-2 receptor Nectin-1 under the control of CLOCK coincided with an increase in viral titer suggesting that HSV-2 infection is regulated by the host circadian clock.
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