During the early stages of infection, adenovirus particles induce the MyD88-dependent production of RANTES, IP-10, and MIP-1 [53] . The cytokines produced enhance both sensitivity to LPS and the production of TNF-α. TNF-α suppresses the formation and maturation of virus particles, and induces apoptosis of infected cells. TNF-α also promotes the chemotaxis and maturation of dendritic cells. The induction of TNF-α is considered to be a host defense response. On the other hand, the adenovirus E1A and E3 proteins inhibit TNF-α-induced apoptosis. The receptor internalization and degradation (RID) complex, which consists two E3 products, E3(10.4 k)/RIDα and E3(14.5 k)/RIDβ, suppresses cell surface expression of Fas, TNF-related apoptosis-inducing ligand (TRAIL) receptor 1, TRAIL receptor 2, and TNF receptor 1 [54, 55] . This results in the shutting down of the TNF-α-mediated signaling pathways in the infected cells. RID also suppresses the TLR4 signaling pathway. LPS-induced MCP-1 and IL-8 production are suppressed through the inhibition of NF-κB and AP-1 activation [56] . RID does not alter the expression levels of TLR4, and so is thought to affect other components of the TLR signal transduction pathway.