Therefore, although HSV gD may compete with both LIGHT [5] and BTLA [7] for binding to HVEM and/or rapidly downregulate surface expression of HVEM to decrease LIGHT- or BTLA-mediated signaling [18], our observations of increased chemokine responses after infection with virus mutated to remove interaction with HVEM are consistent with the notion that wild-type gD may interfere with a proinflammatory signal. Here, BTLA is linked to infection.