This explains (1) recruitment of HIV-1 permissive monocytes/macrophages and CD4+ T cells at the site of infection for new rounds of replication (feed-back loop model), (2) induction of HIV-1 co-receptor CXCR4 by CCL2 (38), (3) CCL2-mediated polarization of helper T cell (Th0) toward Th2 phenotype (39), (4) IL-4 induction CXCR4 expression on resting CD4 T cells (40), and (5) enhanced HIV-1 progeny release by CCL2 (34). The gene discussed is CCL2; the disease is infection.