This may be even more likely in HIV-2 since in this model the usage of cell receptors seems to be much more complex, as suggested by the identification of HIV-2 strains characterized by: (i) a CCR5/CXCR4-independent entry; (ii) a broader coreceptor usage compared to HIV-1; and (iii) a CD4-independent infection of host cells (reviewed in [72-74]). Here, CXCR4 is linked to infection.