It has been proposed that KSHV infection plays a major role in the recruitment of inflammatory cells to the KS lesions by upregulating the expression of chemotactic chemokines and, consistent with this notion, latent infection of vascular endothelial cells with KSHV has been known to upregulate the expression of several cellular chemokines, such as IL-8, GRO-1, MCP-1, NAP-2, CCL5/RANTES and CXCL16 [32,15,21,18,33,22]. This evidence concerns the gene CCL2 and disease arising from reactivation of latent virus.