Modulatory molecular mechanisms have been described for herpes simplex virus type 1 (HSV-1) infection; interactions between viral glycoprotein HSVgD and herpes virus entry mediator (HVEM) were found to promote Treg proliferation; in turn, preactivated Tregs upregulate HVEM, inducing positive feedback between both (187), although other authors argue that Treg may unexpectedly facilitate early immune responses in HSV-infected mice by orchestrating homing of effector cells to the site of infection (188). The gene discussed is TNFRSF14; the disease is infection.