HIV-associated neurocognitive disorder (HIV-ASCD) is a neurological disorder associated with HIV and AIDS, including neurological disorders of varying severity. HIV-associated neurocognitive disorder is associated with metabolic encephalopathy caused by HIV infection, fueled by immune activation by macrophages and microglia, as these cells are actively infected by the virus and secrete neurotoxins produced by humans and viruses. The main features of HIV-associated neurocognitive disorder are disabling cognitive impairment accompanied by motor impairment, speech problems and behavioral changes. Cognitive impairment is characterized by mental slowness, memory problems and poor concentration. Motor symptoms include loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and reduced emotional and spontaneous responses. At the histopathological level, it is characterized by infiltration of monocytes and macrophages into the central nervous system, neuroglial degeneration, myelin sheath pallor, dendritic cell damage and neuronal loss. HAD typically occurs years after HIV infection and is associated with low CD4+ T-cell levels and high plasma viral load. It is sometimes considered the first sign of AIDS onset. The prevalence is 10–24% in Western countries and has been observed in only 1–2% of infections returning to India. With the advent of highly active antiretroviral therapy (HAART), the incidence of HAD has declined in developed countries, although its prevalence is increasing. HAART has the potential to suppress or delay the onset of HAD in HIV-infected individuals, as well as improve mental function in those with pre-existing HIV-associated dementia. Dementia occurs when an individual develops a progressive and severe neurocognitive deficit that significantly interferes with daily functioning. The patient subsequently loses the ability to work and may be unable to care for themselves. Before the condition progresses to this degree, a patient can be considered to have mild neurocognitive disorder. HIV-associated cognitive deficits affect the domains of attention, memory, verbal fluency, and visuospatial construction. For memory in particular, decreased activity in the hippocampus alters the basis of memory encoding and affects a number of mechanisms including long-term consolidation. The severity of deficits in different domains varies depending on whether a patient is treated with H-A-R-T or monotherapy. Studies have shown that patients experience cognitive deficits with dysfunction in fronto-striatal circuits including associated parietal regions, which may play a role in the observed deficits in visuospatial function. In addition to cognitive deficits, the development of psychological dysfunction can be observed. For example, HIV-infected patients have high rates of clinical depression and alexithymia, which is the difficulty in processing or recognizing one’s own emotions. Patients also have difficulty recognizing facial expressions. The severity of cognitive deficits is exacerbated in later stages of HIV infection if a patient is not treated with a combination of highly active antiretroviral therapies. Early HIV patients show mild difficulties with concentration and attention. In advanced HIV-associated dementia, speech impairment, motor dysfunction, and disturbances in thinking and behavior can be observed. In particular, slower motor speeds have been associated with enlargement of the right putamen. HIV-associated neurocognitive disorder can be diagnosed using clinical criteria after other etiological possibilities have been considered and ruled out. The severity of neurocognitive disorder correlates with CD4, suggesting that early treatment to prevent HIV-induced immunosuppression may help prevent the development of HIV-associated neurocognitive disorders. Mother-to-child transmission during pregnancy is the most common form of HIV infection in children and has been associated with an increased risk of death and developmental delay. Neurological disease has been observed in children with AIDS as a result of HIV-1 infection. HIV-1 can infect the central nervous system of newborns with HIV within weeks of initial infection, causing neurological damage and cell death. Although neuronal dysfunction is associated with HIV infection of the CNS, the pathogenesis of the neurological disorders remains unclear. The main cells infected by HIV-1 in the nervous tissue include microglia, astrocytes, and macrophages, while neurons are rarely infected. Susceptibility to HIV-1 infection, along with viral replication in neurons and glia, is a function of cell differentiation, and is more likely to occur in immature progenitor cells than in differentiated cells. Several resolvable signals, such as cytokines, have been proposed to modulate susceptibility and contribute to viral latency or viral replication during organ development. In fact, cells during CNS development are under the control of environmental factors that provide guidance signals to neuronal cell targets. By regulating the survival, differentiation, and maintenance of specific functions of neuronal and glial progenitor cells, these extracellular signals can influence various stages of CNS development as well as mediate viral-cell interactions in the developing brain. In addition to cytokine production, HIV-1-infected monocytes and astrocytes are capable of producing a number of soluble mediators, including viral proteins such as gp120 and Tat, which can exert deleterious effects on both developing and mature neural tissues. Furthermore, molecules such as platelet-activating factor and prostaglandins, produced by functional interactions between microglia/macrophages and astrocytes, have been shown to mediate cellular damage in primary neuronal cultures and neuronal cell lines with an immature phenotype. Together, these observations suggest that the mechanism by which the virus modulates CNS development and induces immature brain disease depends on the modulation of the production of soluble bioactive compounds. Several mediators that may exert neurotoxic effects have been identified in several model systems, including inflammatory cytokines, viral proteins and neurotoxic metabolites. As a result, the complex interplay between different mediating factors may modify the function of developing and mature cells, responsible for neurological disorders, and influence their survival.