Our data extend these findings and demonstrate that LPS treatment, as well as infection with the sexually transmitted pathogen GC or the gut-associated microbe E. coli, represses HIV-1 expression in MDMs through the TLR4-mediated, TRIF-dependent production of type I IFNs and the subsequent recruitment of IRF8 to the HIV-1 ISRE (Fig. 7). This evidence concerns the gene TLR4 and infection.