pregnancy is the dominant mode of acquisition of hiv infection in children and has been associated with an increased risk of mortality and developmental delay. children with aids appear to have neurological diseases as a consequence of hiv-1 infection. in hiv-1 infected newborn and children, central nervous system (cns) is infected with hiv-1 weeks after primary infection, causing neuronal damage and cell death. although neurological dysfunctions have been associated to hiv infection of the cns, it is unclear how the pathogenesis of neurological disorders has been established. the main cells infected by hiv-1 in the nervous tissue are the microglia, astrocytes and macrophages, whereas infected neurons have been rarely observed. the susceptibility to hiv-1 infection and replication in neuronal and glial cells is a function of cellular differentiation, and it is more likely in immature precursors than with differentiated cells. several soluble signals, such as cytokines, have been described to modulate susceptibility and can further contribute in supporting virus latency or virus replication during organ development. in fact, within the developing cns, cells are under the control of environmental factors that provide instructive signals to neural cell targets. by regulating the survival, differentiation and maintenance of specific functions of neuronal and glial precursors, these extracellular signals can influence many steps of the cns development and concur in controlling virus-cell interactions in the maturing brain. in addition to the production of cytokines, hiv-1 infected mononuclear cells and astrocytes can produce a number of soluble mediators, including viral proteins such as gp120 and tat, that can exert damaging effects on both developing and mature neural tissues. moreover, molecules such as the platelet activating factor (paf) and prostaglandins, which are produced upon microglia/macrophages and astrocytes functional interactions, have been reported to mediate cell damage in primary neural cell cultures and neural cell lines with immature phenotype. taken together, these observations suggest that the mechanism by which the virus can alter cns development and induce pathology in the immature brain may depend upon the altered production of soluble bioactive compounds. several potentially neurotoxic mediators have been identified in different model systems, including inflammatory cytokines, viral proteins and neurotoxic metabolites. thus, it is likely that a complex interaction of several mediators may alter the function and survival of actively developing and maturing cells, responsible for the neurologic disorders.