Therefore, low production of ROS can also contribute to our hypothesis related to innate immune quiescence and resistance to HIV-1 infection, because ROS production is involved in both pro-inflammatory cytokine production and HIV-1 LTR activation via post-translational control of NF-κB [58] and up-regulation of CD11b expression [59]. Here, NFKB1 is linked to HIV-1 infection.