HLA polymorphisms in Nigerians

Abstract

The HLA class I and class 11 phenotypes of a panel of 114 unrelated Nigerians have been determined. The panel was tested for all the known class I antigens and comparisons of the HLA-A and -B frequencies with those of other African Negroid populations revealed some differences. Only limited comparisons could be made for the HLA-DR and -D frequencies as these are not available for any well-defined African Negroid population. The data concerning the class I1 antigens of this panel are the most interesting. Half of the DRwll-positive panel members are DQw3 negative and DQwl positive. in addition, there is dissociation of some HLA-D and -DR specificities, a number of panel members are positive for an HLA-D specificity and are negative for the corresponding HLA-DR specificity. Our results show the value of population studies in the investigation of the relationship between the different HLA class 11 antigens.

Subtype-Specific Patterns in HIV Type 1 Reverse Transcriptase and Protease in Oyo State, Nigeria: Implications for Drug Resistance and Host Response

“…33 We found subtypespecific polymorphisms in RT within epitopes for HLA B7 and B35 (Fig. 2), which, interestingly, have relatively high allelic frequencies (11% and 7%, respectively) in the Southern part of Nigeria 47,48 Our previous studies have previously demonstrated that the CTL response is abrogated with the S162A mutation in subtype A individuals. 49 This polymorphism is found in a majority of CRF02_AG viruses within the B7 epitope.…”

“…55 It is conceivable that subtype-specific polymorphisms exist within CTL and T-helper epitopes for HLA proteins that are common in the regions where these subtypes predominate. HLA B35 and B7 occur at similarly high levels in whites, 47,56 and have been associated with increased rates of disease progression and higher viral loads, respectively. 54,57 We suggest that the relatively high frequencies of these antigens within various populations contribute to the selective pressures that lead to the development of immune escape variants, which then persist in these populations.…”

Human leukocyte antigen class I haplotypes of human immunodeficiency virus–1–infected persons on Likoma Island, Malawi

“…The most protective alleles identified have been B27 and B57, which are infrequent in our Malawian cohort and other studies of Africans, but more commonly found in American and European Caucasians. B35 has been associated with more rapid disease progression, and appears to be lower in frequency in our cohort (about 2%) compared to Caucasian groups where it runs from about 7 to 10% [10, 13, 23], although different B35 subtypes vary in their influence on disease [36], and we do not have breakdowns for B35 subtypes. Given the relatively recent initiation of the HIV-1 pandemic, it is likely that the virus has not yet influenced HLA frequencies in humans, but the pre-existing rates of certain HLA alleles may affect the spread of the virus in different human populations.…”

“…The B53 allele, which is particularly common in the Likoma Island cohort at about 12%, has been suggested to have a strong protective benefit against severe malaria [25]. B53 has a low frequency of <1% in Caucasians from South Africa [10], Britain [13], and Europe [23], as well as Japanese [23]. Interestingly, in other sub-Saharan African populations, B53 varies considerably in frequency, with a reported frequency of <1% in Namibian San Bushmen [9] and Guineans [18], but a frequency of about 22% in Nigerians [13], perhaps reflecting the distribution of malaria predominately across central Africa.…”

“…HLA data from our cohort were compared to previously published HLA frequencies in different ethnic populations, including Botswanans [7], Congolese [8], Namibian San Bushmen [9], South African Xhosas and Whites [10], South African Blacks who were primarily Zulu [11, 12], Nigerians [13], Zimbabwean Blacks [14], Gambians [15], Malians [16], Ugandans [17], Equatorial Guineans [18], Rwandans [19], Zambians [20], United States American Blacks [15, 21, 22], South African Whites [10], British Whites [13], Europeans [23], and Japanese [23]. Only HLA types (low resolution) for which unambiguous and complete comparisons (molecular versus serological typing) could be made across all datasets were utilized (A-alleles 01, 02, 03, 11, 23, 24, 25, 26, 29, 30, 31, 32, 33, 34, and 36; B-alleles 07, 08, 13, 14, 18, 27, 35, 37, 39, 40, 41, 42, 44, 45, 47, 48, 49, 50, 51, 52, 53; C-alleles 01, 02, 03, 04, 05, 06, 07, 08).…”