Abstract
HSV-1 inhibits apoptosis of the infected cell, presumably to increase viral yield. Weaker anti-apoptotic activity was previously reported in laboratory-adapted HSV-2, but not in two low-passage clinical HSV-2 isolates, suggesting that the anti-apoptotic effect might result from adaptation to laboratory growth. We therefore assembled a large panel of clinical strains of HSV-1 and HSV-2. Clinical and laboratory strains of HSV-1 strongly inhibited apoptosis of Jurkat cells, as determined by morphologic change or caspase activation, while clinical HSV-2 strains showed no inhibitory activity in Jurkat cells. These findings suggest fundamental differences between HSV-1 and HSV-2 in their manipulation of host cell apoptosis.
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