Does herpes simplex virus type I require productive infection to induce tissue factor in human umbilical vein endothelial cells?
HSV-1 induces PCA in HUVEC which is clearly TF-dependent; this response does not require viral replication. These data indicate increased complexity in HSV interactions with vascular endothelium and imply induction of some procoagulant functions by nonproductive infection.
Annual decline of GFR is an independent risk factor for CVD. Serial measurement of both creatinine and proteinuria would be better to predict the incidence of CVD in the general population.