This view is supported by the finding that a panel of commercially available murine mAbs, whose reactive sites were localized to the ECL1/ECL2 domains or the single ECL2 domain of CXCR4, also showed similar, but less effective suppressive effects on infection with both the X4 and R5 HIV-1 and enhanced MIP-1α and β production under the same culture conditions presented herein (data not shown). The gene discussed is CXCR4; the disease is infection.