Chapter 16

Acquired immune deficiency syndrome (AIDS) was discovered in 1981 as an infectious disease of homosexual men transmitted by sexual intercourse. The human immunodeficiency virus (HIV) was soon discovered and shown to be the causative agent, and additional risk groups and modes of infection were identified. The virus could also be transmitted by blood transfusions and contaminated needles. HIV infects a small population of helper T cells and the helper T cell count decreases, at first slowly, and then, after a variable length of time, precipitously. The patient typically loses weight, has chronic diarrhea and is susceptible to multiple infections and cancers. There are many puzzling aspects of HIV pathogenesis within the framework of the conventional viewpoint that HIV kills helper T cells directly. An alternative concept is that HIV triggers autoimmunity, and was first published by Ziegler and Stites237, by Andrieu et al.238, and by Shearer239, based on the fact that there is serological cross-reactivity between HIV components and MHC class II. There is however no evidence of anti-MHC class II antibodies in AIDS patients. My colleagues and I have developed an autoimmunity theory of AIDS pathogenesis in the context of the symmetrical network theory, including the resolution of the I-J paradox described in chapter 13. In this chapter I will first outline the autoimmunity model, then discuss the ways in which it accounts better for many aspects of the disease than the conventional model, in which HIV kills helper T cells directly. The model is based on the idea that there is an MHC class II image centre-pole also in humans, analogous to the I-J centre-pole in mice, and that this is susceptible to autoimmunity triggered by HIV.