Moreover, TLR7 and TLR8 (25–27) respond to HIV-1 infection by triggering type I IFN (28) or interleukin-1b production (29); stimulation of both these receptors has been shown to lead to increased HIV-1 replication in productively infected cells (30), whereas their inhibition has the opposite effect (31) suggesting that the dampening of NF-κB activity mediated by the CACTIN upregulation which we observed in the present study could function to suppress viral replication. The gene discussed is CACTIN; the disease is HIV-1 infection.