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Common epitope on HIV p24 and human platelets
A W Hohmann1, K Booth, V Peters
1Department of Clinical Immunology, Flinders Medical Centre, Bedford Park, Australia.
Lancet (London, England)
|November 20, 1993
Summary
Human immunodeficiency virus (HIV) may trigger autoimmune responses in AIDS by mimicking human antigens. A specific antibody showed cross-reactivity with platelets, suggesting a mechanism for HIV-associated thrombocytopenia.
Area of Science:
- Immunology
- Virology
- Hematology
Background:
- Autoimmunity is observed in Acquired Immunodeficiency Syndrome (AIDS).
- Human Immunodeficiency Virus (HIV) may possess antigens that mimic human proteins.
- This mimicry could be a potential cause of autoimmune phenomena in HIV infection.
Purpose of the Study:
- To investigate the potential of HIV antigens to induce autoimmune reactions.
- To explore the cross-reactivity of an antibody raised against HIV p24 with human cellular components.
- To understand the mechanism behind HIV-associated autoimmune-like thrombocytopenia.
Main Methods:
- Development of a mouse monoclonal antibody (VIC8) against HIV p24 antigen.
- Testing the cross-reactivity of VIC8 with human platelets.
- Assessing the effect of recombinant p24 antigen on antibody-platelet binding.
- Comparing VIC8 binding to platelets from HIV-infected patients and healthy individuals.
Main Results:
- The VIC8 antibody, raised against HIV p24, demonstrated cross-reactivity with human platelets.
- Binding of VIC8 to platelets was inhibited by recombinant p24 antigen.
- VIC8 exhibited reduced binding to platelets from HIV-infected individuals compared to healthy controls.
- No correlation was found between VIC8 binding, p24 antigenaemia, disease stage, or platelet count in HIV patients.
Conclusions:
- HIV's antigenic mimicry of human components is further exemplified by this cross-reactivity.
- This phenomenon may play a significant role in the pathogenesis of HIV-associated autoimmune-like thrombocytopenia.
- Further research into HIV antigenic mimicry is warranted to understand associated autoimmune conditions.