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HIV induces modulation of functionally important cellular antigens
M Wrightham1, A Schimpf, T H Pennington
1Department of Microbiology, University of Nottingham, UK.
Clinical and Experimental Immunology
|July 1, 1991
Summary
HIV-1 infection alters T cell antigen expression, increasing intercellular adhesion receptor LFA-1 (CD11a/CD18) and HLA-DR while decreasing CD7. These changes, specific to the virus isolate, impact HIV pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human Immunodeficiency Virus type 1 (HIV-1) infects T lymphocytes, crucial components of the immune system.
- Understanding how HIV-1 alters cellular functions is key to comprehending viral pathogenesis and developing treatments.
Purpose of the Study:
- To investigate the modulation of cellular antigen expression in T lymphoblastoid CEM cells following HIV-1 infection.
- To determine the role of specific viral isolates and components in these phenotypic changes.
Main Methods:
- Infection of CEM cells with HIV-1 isolates (IIIB and CBL-1).
- Immunocytochemical techniques to detect and quantify cellular antigens (CD4, LFA-1, HLA-DR, CD7).
- Treatment of uninfected cells with recombinant viral proteins (gp120, p24).
Main Results:
- HIV-1 IIIB isolate infection induced LFA-1 (CD11a/CD18) and HLA-DR expression in cytoplasm and on cell surface.
- HIV-1 IIIB isolate infection down-regulated CD7 antigen expression, making it undetectable.
- Phenotypic changes were dependent on the HIV-1 isolate and not replicated by exogenous gp120 or p24.
Conclusions:
- HIV-1 infection significantly alters T cell surface antigen expression, affecting immune cell interactions.
- The observed modulation of LFA-1 and CD7 may contribute to HIV pathogenesis and immune dysfunction.
- Virus isolate-specific effects highlight the complexity of HIV-1-host cell interactions.