The human major histocompatibility complex and HIV-1 pathogenesis
Mann, D. L., Carrington, M. N., & Kroner, B. (1994). The human major histocompatibility complex and HIV-1 pathogenesis. AIDS, 8(Suppl 1), S53-S60.
Antibodies reacting with lymphocytes were first recognized some 35 years ago in sera from multiple-transfused individuals and in sera from women who had been pregnant [1-3]. The cell surface structures detected by these antibodies, the HLA calss I and class II antigens, were recognized as strong determinants of histocompatibility that are under the genetic control of several closely linked loci, which map to the short arm of chromosome 6 in a region known as the major histompatibility complex (MHC) [4-7]. Most, if not all, mammalian species have an MHC. In studies in the guinea pig and mouse, McDevitt and Benacerraf and colleagues [8,9] demonstrated that the MHC contains genes that regulate the immune response, a fundamental concept in immunology. Over the past two decades the genetic organization and the structure and function of the gene products of the human MHC have been eludicated.
Recognition of the extensive polymorphism in the HLA system led to studies designed to determine whether particular alleles of the class I and class II loci are associated with various human diseases. Possibly most known diseases have been tested for associations with HLA determinants. Indeed, some such diseases have been described, for the most parth those considered to involve autoimmune processes. Surprisingly, few infectious diseases have demonstrated associations with HLA alleles, probably because of the difficulty in documenting exposure an differences in individual responses to the pathogen and disease outcome. Each component may be regulated separately or collectively by HLA alleles that have different functional properties. Infectious diseases are a postulated mechanism that drives and maintains MHC polymorphism by a process of selection.