The clearly lower inhibitory potency of wild-type GRFT and its mutant variants against DC-SIGN-directed virus capture versus cell-free virus infection of CD4+ T-lymphocytes and DC-SIGN-directed transmission of HIV to CD4+ T-lymphocytes may suggest that DC-SIGN recognizes, at least partially, different glycan epitopes on gp120 than GRFT and/or recognizes some glycan epitopes more efficiently than GRFT and therefore, relatively high GRFT concentrations are needed to prevent DC-SIGN-mediated HIV-1 capture. This evidence concerns the gene CD4 and viral infectious disease.