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Updated: Apr 13, 2026

Amplifying and Quantifying HIV-1 RNA in HIV Infected Individuals with Viral Loads Below the Limit of Detection by Standard Clinical Assays
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Amplifying and Quantifying HIV-1 RNA in HIV Infected Individuals with Viral Loads Below the Limit of Detection by Standard Clinical Assays

Published on: September 26, 2011

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Molecular virology and immunology of HIV infection

Javier Chinen1, William T Shearer

  • 1Allergy and Immunology Program, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.

The Journal of Allergy and Clinical Immunology
|August 10, 2002
PubMed

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.

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