title: Can we find a solution to the human immunodeficiency virus/acquired immune deficiency syndrome controversy? Is acquired immune deficiency syndrome the consequence of continuous excessive stressing of the body?
abstract: The time of re-evaluation of the role of human immunodeficiency viruses in the pathogenesis of acquired immune deficiency syndrome has now come, now that methods are available for the direct detection of human immunodeficiency viruses and for the detection of cellular anti-human immunodeficiency virus immune reactions. It has been shown that human immunodeficiency virus infections are common among anti-human immunodeficiency virus antibody negative high-risk individuals. The disease is brought under control by cellular immune reactions and the anti-human immunodeficiency virus antibody test remains negative. Apart from proof that infection with human immunodeficiency viruses has occurred, a positive result in an anti-human immunodeficiency virus-antibody test is also an indication of an independent immunosuppression state. According to the definition of the Centers of Disease Control classical acquired immune deficiency syndrome is the consequence of infection with human immunodeficiency virus in association with continuous excessive stress, such as observed in the known risk groups. At the center of the pathogenetic process is hypercortisolism-determined damage of T lymphocytes, in which insufficiency of thymus is prominent. For this reason, in our view, there are indications for shifting efforts from the prophylaxis of infection with human immunodeficiency viruses to the prophylaxis of acquired immune deficiency syndrome by reducing stress factors.
authors: Study Group Nutrition and Immunity, Bern, Switzerland.
authors: A
authors: A
authors: Hässig
authors: L
authors: L
authors: Wen-Xi
authors: K
authors: K
authors: Stampfli
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology* / Q000276:immunology; D000818:Animals; D005260:Female; D006678:HIV / Q000276:immunology / Q000472:pathogenicity; D015483:HIV Antibodies / Q000097:blood; D015658:HIV Infections / Q000209:etiology* / Q000276:immunology; D006467:Hemophilia A / Q000150:complications; D018451:Homosexuality, Male; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D008297:Male; D051379:Mice; D008954:Models, Biological; D012307:Risk Factors; D013312:Stress, Physiological / Q000150:complications / Q000276:immunology; D019966:Substance-Related Disorders / Q000150:complications; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D065227:Transfusion Reaction
chemical_list: D015483:HIV Antibodies