CXCR4 and infection: Although a definitive model explaining the differential capacity of R5 and X4 viruses to replicate in CD4+ lymphocytes cannot be still drawn, it is important that the search for correlates of such a relevant difference between these two amazingly similar pathogens with so different outcomes for human health (if HIV-1 could only rely on CXCR4 the infection and disease would likely be much more contained and preventable) will still continue.