The Role of Chronic Viral Infection in Immunologic Disease

Abstract

We know a fair amount about how immunologic disease develops and how immunologic reactions trigger humoral and cellular mediators to produce tissue injury. This knowledge has accumulated over the past two decades largely because of the technological and conceptual developments in the field of immunology. These developments have allowed us, first, to quantitate the very basic elements of immunologic reactions: the presence and class of immunoglobulin molecules, the components of complement, and the various kinds of lymphocytes and, second, to determine in which disease states abnormalities of these elements occur. We have been able to link immunologic abnormalities with diseases that, 20 years ago, completely eluded our understanding. Present assays for immune complexes, for auto-antibodies and for abnormally reactive lymphocytes provide the results suggesting specific immunopathologic mechanisms at work in human diseases such as glomerulonephritis, rheumatoid arthritis, systemic lupus erythematosus, a variety of vasculidites, thyroiditis and many other endocrine abnormalities, hepatitis, myasthenia gravis and probably less clearly understood diseases such as multiple sclerosis and subacute sclerosing panencephalitis. In spite of this combination of very sophisticated immunologic information and suspicion, which is really what it is, we have very little understanding of etiologic agents in most of these diseases.