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

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.