Great progress has been made with respect to our understanding of the immunopathogenesis of AIDS and the infectious agent, HIV, that causes the disease. HIV, a human retrovirus with tropism for CD4⁺ T cells and monocytes, induces a decrease of T-cell counts, T-cell dysfunction, and, ultimately, immunodeficiency.

 HIV also causes B-cell dysfunction characterized by polyclonal activation, hypergammaglobulinemia, and lack of specific antibody responses. Chemokine receptors—mainly CCR5 and CXCR4—have been found to be necessary for viral entry into the host cell, a step that can be inhibited by chemokine-related molecules that are ligands for those receptors. After HIV infection, a strong cellular immunity develops and partially controls viral replication.

 It can take several years for HIV infection to become clinically evident. Studies in long-term nonprogressors have shown the determinant roles of both helper and cytotoxic T cells in the control of HIV disease. Advances in HIV immunology research are currently being applied in the development of prophylactic and therapeutic vaccines.

Warm Regards,
Jessie
Journal Manger
Journal of Clinical Immunology and infectious diseases
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