Cerebrospinal fluid western Blot profiles in the evolution of HIV-1 pediatric encephalopathy.

In order to obtain information on neurologic AIDS, 54 white caucasian children infected by nosocomial route with a median age of 46.2 +/- 7 months were followed up prospectively for a median of 12 months with three months Denver tests neurologic evaluation and six months serologic investigations in CSF and sera. Paired CSF and serum samples, collected on the same day, from children with AIDS encephalopathy, were analysed for the permeability of the blood brain barrier (BBB) and for intrathecal production of anti HIV specific antibodies. A prospective follow-up and repeated comparison of WB profiles and the presence of anti V3 antibodies in CSF and sera was done, as well as an evaluation of the modification in the CSF antibody specificity (anti gag Western Blot scoring) with disease progression. An increased intrathecal synthesis of IgG was recorded in all subjects, in spite of an unaltered BBB permeability. No significant differences were recorded for the anti gag score in the serum samples, which was stable between 9.1-10.4. By contrast, the score for CSF samples decreases significantly with disease progression, from 8.7 in children without encephalopathy, to 6.5 in those with stationary disease and 3.6 in the progressive encephalopathy group. A strong correlation was found between the level of anti p24 antibodies determined by ELISA and the anti gag score quantified by WB for the same CSF samples. The p24 antigen was found to be positive only in 3 cases, even after immune complex dissociation. Anti V3 antibodies were not detected in CSF samples from patients with functional BBB. The decline in anti-gag antibody reactivity in CSF is an early indicator of disease progression, reflecting a severe course of neurological impairments. The absence of anti V3 antibodies in the CSF samples suggests that the PND of neurotropic strains mapped in distinct positions into the V3 loop. These results reflect the selection of antigenic escape mutants which evolve in the CNS, distinct from the blood lymphotropic isolates.