Thus, in our model we suggest that IL-6, IL-8, TNFα, and IL-1β might be acting synergistically at different levels (i.e., modifying the cellular environment and/or by enhancing transcriptional and/or post-transcriptional mechanisms) to promote, at least transiently, the productive infection of unactivated CD4+ T cells. This evidence concerns the gene CXCL8 and infection.