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Host cell components affect the sensitivity of HIV type 1 to complement-mediated virolysis
M Saifuddin1, M Ghassemi, C Patki
1Department of Immunology/Microbiology, Rush University, Chicago, Ilinois.
AIDS Research and Human Retroviruses
|July 1, 1994
Summary
Host cell components significantly impact HIV-1 susceptibility to complement-mediated virolysis. Phosphatidylinositol-linked proteins like membrane inhibitor of reactive lysis (MIRL) and decay-accelerating factor (DAF) on host cells confer resistance to viral lysis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- The complement system plays a crucial role in innate and adaptive immunity.
- HIV-1 interaction with the complement system is complex and influenced by viral and host factors.
- Understanding host cell contributions to HIV-1 complement resistance is vital for therapeutic strategies.
Purpose of the Study:
- To investigate how host cell components affect HIV-1 susceptibility to complement-mediated virolysis.
- To determine the role of specific complement regulatory proteins (CRPs) expressed on host cells in HIV-1 complement resistance.
- To assess the impact of phosphatidylinositol (PI)-linked proteins on HIV-1 complement-mediated lysis.
Main Methods:
- Expression of HIV-1 (pNL4-3) in various human cell lines and peripheral blood mononuclear cells.
- Assessment of complement-mediated virolysis using HIV antibody-positive patient serum and monoclonal antibodies.
- Quantification of complement receptors (CR1, CR2, CR3), complement control proteins (MIRL/CD59, DAF/CD55), and HLA-DR on host cells.
- Evaluation of HIV derived from wild-type and mutant cell lines (PI-linked protein deficient).
Main Results:
- HIV-1 produced in H9 cells showed susceptibility to complement-mediated lysis with specific antibodies.
- Inverse correlation observed between host cell expression of MIRL and DAF and HIV-1 sensitivity to complement.
- HIV derived from a mutant cell line deficient in PI-linked proteins (MIRL, DAF) was more sensitive to complement-mediated virolysis (antibody-dependent and independent).
- Direct evidence of MIRL and DAF on viral surfaces, as anti-MIRL or anti-DAF antibodies induced complement-mediated virolysis.
Conclusions:
- Host cell type significantly influences HIV-1 susceptibility to complement-mediated virolysis.
- PI-linked complement control proteins (MIRL and DAF) on the host cell surface play a critical role in conferring resistance to HIV-1 complement-mediated lysis.
- These findings highlight the importance of host-virus interactions in viral immune evasion.