Autodestructive Host Immune Reactions

Autodestructive Host Immune Reactions

Autodestructive Host Immune Reactions

Circulating virus-antibody complexes facilitate viral infectivity. Peripheral blood leucocytes have receptors for the Fc region of IgG. This allows greater adsorption of virus-antibody complexes than of free viral particles. If the virus-antibody complexes have nonneutralizing antibody, then infection may occur even in non-permissive cells.

Virus-antibody complexes in the circulation, and 1heir deposition in tissues, can initiate severe inflammatory diseases However, -mere, presence of virus-antibody complexes is not sufficient to produce the disease. Host genetic factors and the ability of the virus to replicate within the tissue sites of the complex deposition also influence the frequency, severity, and tissue location of the disease.

Besides virus antibody complexes also activate the complement system. This in turn generates large amounts of inflammatory mediators, and initiates widespread intravascular coagulation. In severe cases, over 80 per cent of serumCgandC5 - are activated. The inflammatory response to the circulating virus-antibody complexes induces significant tissue destruction. This tissue destruction, associated with many viral infections, is due to a combination of virus and host effects.

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