The Role of the Complement System in Host Defense Against Virus Diseases

  • Neil R. Cooper

Abstract

Complement is an effector system capable of mediating a number of biological activities. Most familiar is the ability of the system to mediate the lytic destruction of many kinds of cells including bacteria and viruses surrounded by lipid membranes. Apart from such direct effects on a virus or other pathogens, the activated complement system also facilitates interactions with various effector cells including neutrophils, monocytes, basophils, mast cells, and lymphocytes. Depending on the effector cell involved, complement may trigger the release of histamine and other secondary mediators, stimulate oxidative metabolism, activate intracellular processes, initiate directed motion, facilitate phagocytosis, and modulate immunological responses and immune reactions (Fig. 1). Although complement can thus mediate numerous reactions in vitro, the most important in vivo role in diseases, including virus diseases, is probably related to the system’s ability to produce an acute inflammatory response and to function as an opsonin in facilitating phagocytosis. Thus, activation of complement in a localized environment leads to changes in capillary permeability, edema, alterations in vessel contractility, and directed migration of leukocytes into the area. The phagocytic cells infiltrating the area of complement activation become fixed to specific opsonic sites on the complement molecules, which are in turn attached to the surface of the pathogens.

Keywords

Permeability Migration Lymphoma Influenza Histamine 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Cooper NR (1983) Activation and regulation of the first complement component (C1). Fed Proc 42:134–138PubMedGoogle Scholar
  2. 2.
    Pangburn MK (1983) Activation of complement via the alternative pathway. Fed Proc 42:139–143PubMedGoogle Scholar
  3. 3.
    Cooper NR (1979) Humoral immunity to viruses. In Fraenkel-Conrat H, Wagner RR (eds) Comprehensive Virology. Plenum Press, New York p 123CrossRefGoogle Scholar
  4. 4.
    Sissons JGP, Oldstone MBA (1980) Antibody-mediated destruction of virus-infected cells. Adv Immunol 29:209–260PubMedCrossRefGoogle Scholar
  5. 5.
    Nemerow GR, Jensen FC, Cooper NR (1982) Neutralization of Epstein-Barr virus (EBV) by nonimmune human serum: Role of cross-reacting antibody to herpes simplex virus (HSV-1) and complement (C). J Clin Invest 70:1081–1091PubMedCrossRefGoogle Scholar
  6. 6.
    Beebe DP, Schreiber RD, Cooper NR (1983) Neutralization of influenza virus by normal human sera: Mechanisms involving antibody and complement. J Immunol 130:1317–1322PubMedGoogle Scholar
  7. 7.
    Cooper NR, Jensen FC, Welsh Jr. RM, Oldstone MBA (1976) Lysis of RNA tumor viruses by human serum: Direct antibody independent triggering of the classical complement pathway. J Exp Med 144:970–984PubMedCrossRefGoogle Scholar
  8. 8.
    Bartholomew RM, Esser AF, Müller-Eberhard HJ (1978) Lysis of oncornaviruses by human serum: Isolation of the viral complement (CI) receptor and identification as p15E. J Exp Med 147:844–853PubMedCrossRefGoogle Scholar
  9. 9.
    Hirsch RL, Winkelstein JA, Griffin DE (1980) The role of complement in viral infections. J Immunol 124:2507–2510PubMedGoogle Scholar
  10. 10.
    Welsh Jr. RM (1977) Host cell modification of lymphocytic choriomeningitis virus and Newcastle disease virus altering viral inactivation by human complement. J Immunol 118:348–354PubMedGoogle Scholar
  11. 11.
    Mayes JT, Nemerow GR, Cooper NR (1983) Alternative complement (C) pathway (AP) activation by Epstein-Barr virus (EBV) infected normal B lymphocytes. Fed Proc 42:5530Google Scholar
  12. 12.
    Norley SG, Wardley RC (1982) Complement-mediated lysis of African swine fever virus-infected cells. Immunol 46:75–82Google Scholar
  13. 13.
    Sissons JGP, Oldstone MBA, Schreiber RD (1980) Antibody-independent activation of the alternative complement pathway by measles virus-infected cells. Proc Natl Acad Sci USA 77:559–562PubMedCrossRefGoogle Scholar
  14. 14.
    Monnell I, Klein G, Lint TF, Lachmann PJ (1978) Activation of the alternative complement pathway by human B lymphoma lines is associated with Epstein-Barr virus transformation of the cells. Eur J Immunol 8:453–458CrossRefGoogle Scholar
  15. 15.
    Perrin LH, Joseph BS, Cooper NR, Oldstone MBA (1976) Mechanism of injury of virus infected cells by antiviral antibody and complement: Participation of IgG, Fab’2 and the alternative complement pathway. J Exp Med 143: 1027–1041PubMedCrossRefGoogle Scholar
  16. 16.
    Weigle WO, Morgan EL, Goodman MG, Chenoweth DE, Hugli TE (1982) Modulation of the immune response by anaphylatoxin in the microenvironment of the interacting cells. Fed Proc 41:3099–3103PubMedGoogle Scholar

Copyright information

© Springer-Verlag New York Inc. 1984

Authors and Affiliations

  • Neil R. Cooper
    • 1
  1. 1.Scripps Clinic and Research FoundationLa JollaUSA

Personalised recommendations