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Human platelets after their contact with influenza virus activate the complement system in autologous serum

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Abstract

Guinea pig erythrocytes that have been exposed to influenza virus activate the alternative pathway through virus-induced desialation of the cells. Neuraminidase treatment of rabbit platelets enhance their clearancein vivo. Washed human platelets were labeled with51Cr exposed to Influenza virus, and resuspended in autologous serum that had been dialyzed against Veronal-buffered saline containing Ca++ and Mg++ (VBS++), VBS containing 8 mM EGTA and 2 mM Mg++ (VBS-MgEGTA) or VBS containing 20 mM EDTA (VBS-EDTA) for 60 min at 37°C. Three per cent51Cr release and no complement consumption were observed in VBS-EDTA serum. In contrast, 6%51Cr release with 37 and 54% decrease in C3 and B hemolytic activities respectively occurred in VBS-MgEGTA serum and 14%51Cr release with 50% decrease in C2 hemolytic activity occurred in VBS++ serum. These results suggest that influenza virus may alter the platelet surface in such a way that both complement pathways might be recruited and the cells be lyzed in autologous serum.

The human complement system is activated by a number of viruses and virus-infected cells through antibody-dependent and independent mechanisms. Guinea pig erythrocytes that have been treated with influenza virus are lyzed in human serum through activation of the classical and of the alternative pathways: activation of the alternative pathway is dependent on an acquired resistance of the cell-bound C3 amplification convertase to control mechanisms that are directly related to desialation of the cells by viral neuraminidase [1]. Since,in vivo, clearance of desialated platelets is enhanced in animal models and since human platelets do not express the C3b receptor-associated inhibitory activity of the complement system, we investigated whether human platelets, after contact with influenza virus, acquire the ability to activate complement in autologous serum.

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References

  1. [1]

    C.R. Lambre, M.D. Kazatchkine, F. Maillet andM. Thibon,Guinea pig erythrocytes after their contact with Influenza virus acquire the ability to activate the human alternative complement pathway through virus induced desialation of the cells, J. Immun.128, 629–634 (1982).

  2. [2]

    J.F. Mustard, D.W. Perry, W.G. Ardlie andM.A. Packham,Preparation of washed platelets from humans, Br. J. Haemat.22, 193–197 (1972).

  3. [3]

    H.J. Rapp andT. Borsos,Molecular Basis of Complement Action. Appleton Century Crofts, New York 1970.

  4. [4]

    S. Ruddy andK.F. Austen,C3 Inactivator of man. I. Hemolytic measurement by the inactivation of cellbound C3, J. Immun.102, 533–539 (1969).

  5. [5]

    D.T. Fearon, M.R. Daha, T.B. Strom, J.M. Weiler, C.B. Carpenter andK.F. Austen,Pathways of complement activation in membrano proliferative glomerulonephritis and allograft rejection, Transplant Proc.9, 729–731 (1977).

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Maillet, F., Lambre, C. & Kazatchkine, M.D. Human platelets after their contact with influenza virus activate the complement system in autologous serum. Agents and Actions 13, 428–430 (1983). https://doi.org/10.1007/BF02176405

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Keywords

  • Influenza Virus
  • Alternative Pathway
  • Complement System
  • Human Platelet
  • Hemolytic Activity