CD8A and myeloid sarcoma: We suggest that the most likely scenario is that a genetically determined quantitative deficiency in the generation of EBV specific CD8+ T cells in vivo allows the accumulation of EBV infected B cells in the CNS in MS and that a vicious circle then ensues whereby the inherently deficient CD8+ T cell response is further compromised by T cell exhaustion31 as a result of the persistent high EBV load in the CNS.