The present investigation was designed to show the incidence of molecular Human Leukocytic Antigen (HLA) class I and class II allelic specificities in plasma cell neoplasia patients, identified by immunohistochemistry, flow cytometry, and high resolution molecular typing. Plasma cell myeloma is the second most common hematological malignancy (13%), comprising 1% of all cancers. Each year, 21000 new cases are diagnosed with a two‐fold prevalence in African Americans in contrast to Caucasians. Our hypothesis is that plasma cell neoplasia have a significant disease association with selected HLA class I and class II alleles. We found that in African American patients diagnosed with plasma cell myeloma (n=10), 50 % expressed HLA‐A*7401 (p= 0.002) and 60% were HLA‐C*0401 positive ( p= 0.004). In patients suspected to have plasma cell neoplasia ( controls n=50), 6% were HLA‐A*7401 positive and 14% expressed HLA‐C*0401. Our results suggest that persons expressing these alleles are more likely to develop plasma cell neoplasia than are those not expressing these alleles. African American patients diagnosed with plasma cell myeloma have significant associations with HLA‐A*7401 and HLA‐C*0401 alleles. Future studies will be directed to identification of HLA class II alleles associated with plasma cell neoplasia.
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 χ2 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, DR11, DRwl2, DQw6 and DQw7, whereas in the Caucasian population A28, Aw66, Bw48, Bw65, Bw70, Cw7, Cw8, 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.
