. HCMV modulates NF-κB activity during the various stages of infection. During the early stages, the membrane glycoproteins gB and gH interact with TLR2 and activate NF-κB [57] . NF-κB then contributes to the induction of proinflammatory cytokines, to the expression of virus immediate early genes, and to the replication of the viral genome. The viral US28 protein, which is a HCMV-encoded chemokine receptor, constitutively activates both NF-κB and phospholipase C signaling pathways [58] . The activated NF-κB mediates the upregulation of the host serine/threonine protein kinase, receptor-interacting protein-like interacting caspase-like apoptosis regulatory protein kinase (RICK).