Therefore, EBV antigens act on the CTLA-4:CD86 transmission pathway by multidirectional induction of the expression of these molecules both in vivo in CLL patients susceptible to EBV infection/reactivation and in vitro, increasing the percentage of CTLA-4+ and CD86+ B lymphocytes among human cells with no detectable amounts of EBV genetic material in PBMCs. Here, CD86 is linked to Epstein-Barr virus infection.