Thus, the potential to prevent infectious replication-competent or replication-defective virus from entering the CNS through blocking the entry of HIV+ CD14+ CD16+ monocytes by targeting their JAM-A and CCR2, and potentially ALCAM, may be a new area to examine in aiming to eliminate viral seeding and replenishment, as well as to reduce the neuroinflammation and neuronal damage that contribute to cognitive deficits. The gene discussed is F11R; the disease is Cognitive impairment.