Molecular mimicry in the pathogenesis of AIDS: the HIV/MHC/mycoplasma triangle

Abstract

The immune defects characterizing infection with the human immunodeficiency virus (HIV) and culminating in the acquired immune deficiency syndrome (AIDS) are the result of a multifactorial disease process, components of which are the occurrence of autoimmune phenomena and opportunistic infection. In this discussion, the observation that both the HIV-1 gp 120 envelope and Mycoplasma genitalium adhesin proteins share an area of significant similarity with the CD4-binding site of the class II major histocompatibility complex (MHC) proteins is placed in this perspective and mechanisms by which interaction within this triad could contribute to the T-cell dysfunction, T-cell depletion, Th1-cell-->Th2-cell shift, B-cell proliferation, hyperglobulinemia and antigen-presenting cell dysfunction observed during the development of AIDS are proposed.