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We measured cerebrospinal fluid (CSF) and serum beta 2-microglobulin (beta 2-M) in Acquired Immunodeficiency Syndrome (AIDS) patients with or without clinical evidence of central nervous system (CNS) involvement. The CSF beta 2-M level was significantly higher than the serum level in AIDS patients with neurological symptoms, but not in AIDS without neurological symptoms, suggesting an increased shedding of this protein in CSF, as a result of rapid cellular turnover within CNS. CSF beta 2-M level increases both in Human Immunodeficiency Virus type 1 (HIV-1) related and in opportunistic CNS syndromes, confirming that beta 2-M is a non specific marker of CNS involvement in AIDS. Nevertheless, the highest CSF beta 2-M values were observed in patients with severe dementia and autoptic diagnosis of multifocal giant cells encephalitis (MGCE) without other opportunistic diseases. This observation could have important implications for monitoring AIDS dementia complex in AIDS patients. Finally, 5 out of 7 (71%) AIDS patients with cryptococcal meningitis showed a decline in CSF beta 2-M level well related to the decrease of cryptococcal antigen (Crypto-Ag) titres and the clinical remission. This data suggests that CSF beta 2-M determination could be used as a useful test in monitoring efficacy of therapy of CNS pathologies in AIDS patients.

The immunohistochemical reactivity of four monoclonal antibodies (MAbs): CVK, 49-5, 49-6 and 63-FH2, raised against the p18 protein of HIV-1 was assessed in tissues obtained from HIV-infected and uninfected individuals. As already reported, all the MAbs specifically labelled follicular dendritic cells (FDC) in lymph nodes from HIV-infected patients with lymphadenopathy, and cells of microglial nodules in the brain from patients with AIDS-related encephalopathy. However, cross-reactivity with normal uninfected tissues was also observed: epithelial cells of the skin, the thymus and tonsils with CVK, and astrocytes in the brain of 49-6 and 63-FH2. Such cross-reactivities suggest that 'molecular mimicry' could exist between p18 of HIV and normal constituents of human cells. This phenomenon could be relevant for the diagnostic use of anti-p18 MAbs on pathological specimens, and it could be of importance in the pathophysiology of HIV infection.

HIV associated subacute, micronodular encephalitis and lymphadenopathy were compared with regard to demonstrable HIV antigens and characterization of HIV antigen expressing cells. In the brain, both gag- and env-coded antigens were confined to cells of micronodular lesions with immunophenotype of monocyte/macrophages (KiM6+, 9.4+, CD4+/-). The micronodular lesions were also infiltrated by some lymphoid cells, predominantly CD8+. In lymphadenopathic nodes, gag-encoded antigens were demonstrable almost exclusively in follicles/germinal centres in association with follicular dendritic cells, whereas env-antigens usually were not found. Follicular involution was related to destruction of follicular dendritic cells and infiltration of CD8+ lymphocytes within the germinal centres. During follicular involution, HIV-gag antigens diminished in parallel with destruction of the network of dendritic reticulum cells. These findings indicate important tissue related differences in HIV expression. In addition, a possible participation of CD8+ cells in the pathogenesis of HIV induced tissue lesions is suggested.

This study deals with the immunohistochemistry of a monoclonal antibody (Mab) raised against the p18 protein of the LAV virus in lymphnodes from 20 cases of persistent generalized lymphoadenopathy (PGL) (2) and 6 of acquired immunodeficiency syndrome (AIDS) (3). In all the PGL cases that have been studied, we observed a very important disruption of the follicular dendritic cell's (FDC) framework in the germinal centers which is associated with the presence of an increased number of Leu2a+ lymphocytes inside the germinal centers. This observation is consistent with the main morphological feature of the lymphnodes in the PGL syndrome which is mainly characterized by lesions of FD cells.