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Influenza virus changes cell-surface glycoproteins including major histocompatibility complex determinants on
F T Rotteveel1, J J Neefjes, H L Ploegh
1Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam.
Human Immunology
|November 1, 1989
Summary
Influenza virus infection increases the binding of antibodies to T cells by reducing sialic acid content, not by altering major histocompatibility complex (MHC) antigen expression. This effect is mediated by viral neuraminidase.
Area of Science:
- Immunology
- Virology
- Biochemistry
Background:
- Major histocompatibility complex (MHC) antigens are crucial for immune responses.
- Influenza virus infection can modulate host immune cell functions.
Purpose of the Study:
- To investigate the impact of influenza virus infection on MHC antigen expression and antibody binding.
- To elucidate the mechanisms behind observed changes in antigen-antibody interactions.
Main Methods:
- Antibody binding assays using T cells and Epstein-Barr virus-transformed B cells.
- Biochemical analysis of MHC antigen levels and sialic acid content.
- Pulse-chase experiments to track sialic acid modification.
- Neuraminidase treatment of cells.
Main Results:
- Influenza infection increased anti-MHC antibody binding to resting and activated T cells.
- No change in MHC antigen levels was detected post-infection.
- A significant decrease in sialic acid content was observed, attributed to viral neuraminidase activity.
- Neuraminidase treatment mimicked the antibody binding changes seen after influenza infection.
Conclusions:
- Influenza virus infection enhances anti-MHC antibody binding to T cells primarily through the reduction of cell surface sialic acid residues by viral neuraminidase.
- The observed effect is not due to an increase in MHC antigen expression.