title: HLA disease association and protection in HIV infection among African Americans and Caucasians.
abstract: In a previous investigation, we demonstrated an increased progression of overt AIDS in the African American population compared to the Caucasian population as reflected by the significantly lower absolute number of CD4+ lymphocytes detected in the African American population in an earlier study. The present study elucidates some of the possible genetic factors which may contribute to disease association or protection against HIV infection. The HLA phenotypes expressed as A, B, C, DR and DQw antigens were revealed by the Amos-modified typing procedure. NIH scoring was utilized to designate positive cells taking up trypan blue. A test of proportion equivalent to the chi 2 approximation was used to compare the disease population (n = 62; 38 African Americans, 24 Caucasians) to race-matched normal heterosexual local controls (323 African Americans, 412 Caucasians). Significant p values were corrected for the number of HLA antigens tested. HLA markers associated with possible protection from infection for African Americans were Cw4 and DRw6, whereas Caucasians expressed none. Disease association markers present in the African American population were A31, B35, Cw6, Cw7, DR5, DR6, DRw11, DRw12, DQw6 and DQw7, whereas in the Caucasian population A28, Aw66, Aw48, Bw65, Bw70, Cw7, DRw10, DRw12, DQw6 and DQw7 were demonstrated. The highest phenotypic frequency for a disease association marker in the study was for HLA-DR5 (62.9%) in the HIV-infected African American population without Kaposi's sarcoma compared to a frequency of 28.9% for the regional control group (p = 0.0012). We conclude that genetic factors do have a role in HIV infection since only 50-60% of those exposed to the AIDS virus will become infected.
authors.affiliation: University of Mississippi Medical Center, Jackson.
authors.forename: J M
authors.initials: JM
authors.lastname: Cruse
authors.forename: M N
authors.initials: MN
authors.lastname: Brackin
authors.forename: R E
authors.initials: RE
authors.lastname: Lewis
authors.forename: W
authors.initials: W
authors.lastname: Meeks
authors.forename: R
authors.initials: R
authors.lastname: Nolan
authors.forename: B
authors.initials: B
authors.lastname: Brackin
mesh_terms: D044383:Black People / Q000235:genetics*; D015153:Blotting, Western; D004198:Disease Susceptibility; D004797:Enzyme-Linked Immunosorbent Assay; D005819:Genetic Markers / Q000235:genetics / Q000276:immunology; D015658:HIV Infections / Q000150:complications / Q000453:epidemiology / Q000517:prevention & control*; D006680:HLA Antigens / Q000235:genetics / Q000276:immunology*; D015234:HLA-A Antigens / Q000235:genetics / Q000276:immunology; D015235:HLA-B Antigens / Q000235:genetics / Q000276:immunology; D015236:HLA-C Antigens / Q000235:genetics / Q000276:immunology; D006683:HLA-DQ Antigens / Q000235:genetics / Q000276:immunology; D006684:HLA-DR Antigens / Q000235:genetics / Q000276:immunology; D006801:Humans; D015994:Incidence; D008137:Longitudinal Studies; D010641:Phenotype; D012514:Sarcoma, Kaposi / Q000150:complications / Q000453:epidemiology / Q000276:immunology; D014481:United States / Q000453:epidemiology; D044465:White People / Q000235:genetics*; D001741:Black or African American
chemical_list: D005819:Genetic Markers; D006680:HLA Antigens; D015234:HLA-A Antigens; D015235:HLA-B Antigens; D015236:HLA-C Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens