CD8A and HIV-1 infection: While resistance of these donors was not due to the production of some other anti-HIV-1 factor such as CD8+T lymphocyte antiviral factor (CAF) [17], it may be possible that treatment with the A120 mAb might induce the hetero-dimerization of CXCR4 and CCR5 which results in resistance to R5 HIV-1 infection.