Abstract

We aimed to assess the effects of human immunodeficiency virus (HIV) encephalitis (HIVE) on the B-lymphocyte population of the brain. We also tested the effects of intravenous opiate drug abuse because this is a major risk factor for infection, with known immunosuppressive properties. Immunohistochemistry was used to identify B lymphocytes in the brains of clinically well-characterized HIV-negative drug abusers, individuals with HIVE, and, for comparison, HIV-negative individuals with encephalitis. Perivascular and parenchymal B lymphocytes were studied in 11 regions of each brain. We found that despite a small apparent rise, the abuse of opiate drugs had no significant effect on the B-lymphocyte population of the brain. Individuals with HIVE were found to have a greater number of B lymphocytes in brain tissue than individuals with acquired immunodeficiency syndrome (AIDS) who had no central nervous system (CNS) pathology. However, in comparison to nonimmunocompromised individuals with encephalitis, the B-lymphocyte population of HIVE brains was greatly reduced. We suggest that this latter finding may be linked to declining CD4 T-lymphocyte levels in end-stage AIDS, and that CD4 T lymphocytes may be required for efficient entry of B lymphocytes to the CNS. The brain B-lymphocyte population correlated well with CD4 T-lymphocyte level in the blood, in cases with viral encephalitis. These findings suggest that systemic immune competence is required to mount a full B-lymphocyte response to viral CNS infections. Furthermore, we suggest that CD4 T lymphocytes may play a key role in the humoral immune response to viral infection of the brain.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.