PubMed1992
At least since the discovery of the acquired immune deficiency syndrome and the "human immune deficiency virus" (HIV) it has been widely accepted, that viruses infect lymphocytes (mainly especially CD 4 positive helper lymphocytes) and can also be responsible for their deletion. However, since the HIV can only be found in a small proportion of the dying lymphocytes, other viruses as well as other (nonviral) cytotoxic agents and mechanisms must be taken into consideration. The conception of involved autoimmune phenomena is being accepted increasingly. Storch's hypothesis put forward in 1975, of primary or secondary viral infection of lymphocytes as pathogenetical principle of autoimmune hepatitis (infected B- and T-lymphocytes stimulate directly or indirectly the antibody synthesis and also trigger abnormal cellular immune reactions) was confirmed. Teleologically regarded, in most cases it remains open if the demonstrable autoantibodies and immune cells are pathogenic, protective, or indifferent for the individual. Analogous to symbiosis and parasitism, this postulate can be extended to pathogenic viral infections. Assuming that the human organism is anxious to remain unharmed and, like viruses maintain its adaptability by a system of multiform control systems one can imagine, that the autoimmunity induced by and therefore directed primarily against viruses can be regarded as "physiological", thus representing a protective mechanism against disturbing exogenous and endogenous factors. It can be considered part of the "prophylaxien" (Holle, 1989). Likewise, in autoimmune hepatitis as well, new findings speak for a participation of several (various) viruses in its aetiopathogenesis. It is hypothesized, that so-called "autogenes" exist which lead to autoimmune disease (like oncogenes involved in the pathogenesis of malignancies).