Immune privilege and HIV-1 persistence in the CNS.

摘要: Summary:  Human immunodeficiency virus-1 (HIV-1) neuroinvasion occurs early (during period of initial viremia), leading to infection a limited amount susceptible cells with low CD4 expression. Protective cellular and humoral immunity eliminate suppress viral replication relatively quickly due peripheral immune responses the level central nervous system (CNS) infection. Upregulation brain protective mechanisms against lymphocyte entry survival (related privilege) helps reduce load in brain. The local compartment dictates evolution as well selection cytotoxic lymphocytes immunoglobulin G specificity. Such status can be sustained until anti-viral fail. Activation microglia astrocytes, or triggers, increases chemokine production, enhances traffic infected into CNS, upregulates resident macrophages, significantly augments spread species. combination these factors leads development HIV-1 encephalitis-associated neurocognitive decline patient death. Understanding immune-privileged state created by virus, microenvironment, ability enhance offer new therapeutic strategies for treatment CNS