Mechanisms of HlV transportation through blood-brain barrier, vascular plexus and interaction with cerebral cells having CD-4-receptors, CCR-5- and CXCR-4-coreceptors were studied. Cerebral damage developed through latent and acute periods also known as HIV-encephalopathy, HIV-associated neurocognitive dysfunction etc. Cerebral lesions are caused by a variety of chemical agents from pro-inflammatory cytokines to toxic HIV-proteins resulting in development of HIV-dementia through several years. Even early stage of this process revealed significant disturbances of glucose metabolism and evoked potentials EEG alterations which can serve as a marker of HIV-infection. Genetic differences ofHWin blood and spinal liquor with different drug resistance were revealed implying a new approach to therapy development.