CD4 and infection: These mechanisms include functional polarization of anti-HIV-1 CD4 T cells toward Tfh rather than Th1 responses, CXCL10 production leading to enhance recruitment of memory CD4 T cells to the sites of viral replication where they fuel chronic viral replication with new HIV-1 target cells (Figure 6,  to ), direct pro-apoptotic and anti-proliferative effects on CD4 T cells (Figure 6, ), as well as TRAIL induction on pDCs licensing them for killing CD4 T cells irrespective of their infection (Figure 6, ) (162, 163).