ABSTRACT
No disponible
Subject(s)
Humans , Female , Adult , Fibromyalgia/complications , Fibromyalgia/diagnosis , Fibromyalgia/therapy , Fatigue Syndrome, Chronic/complications , Fatigue Syndrome, Chronic/diet therapy , Fatigue Syndrome, Chronic/diagnosis , Glutens/adverse effects , Diet, Gluten-Free/trends , Glutens/analysis , Glutens/biosynthesis , Glutens , Iron/therapeutic use , Minerals/therapeutic useABSTRACT
A Nahua Aztec isolated group from Morelos State (Mexico) was studied for their HLA profile. The relationship with other Amerindians and worldwide populations was studied by using 13,818 chromosomes and calculating Nei's chord genetic distances (DA), neighbor-joining dendrograms and correspondence multidimensional values. Three new HLA extended haplotypes were found in our group: A*30-B*49-DRB1*1001-DQB1*0501 (the most frequent one in this population), A*02-B*52-DRB1*1402-DQB1*0301 and A*68-B*61-DRB1*1602-DQB1*0303. Both genetic distances and correspondence analyses clearly show that our Nahua isolated group is genetically close to some of the most ancient groups living in Mexico (Mayans, Zapotecans, Mixtecans). This suggests that Nahua language (Nahuatl) may have been imposed to scattered groups throughout Mexico; otherwise Aztecs may have been living in Mexico long before their postulated immigration in the XII century AD.
Subject(s)
HLA-A Antigens/genetics , HLA-B Antigens/genetics , HLA-DQ Antigens/genetics , HLA-DR Antigens/genetics , Indians, North American/genetics , Gene Frequency , HLA-DQ beta-Chains , HLA-DRB1 Chains , Haplotypes , Humans , Linkage Disequilibrium , Mexico , Phylogeny , Polymorphism, Genetic , Sequence Analysis, DNAABSTRACT
The HLA allele frequency distribution of the Mexican Teenek Indians has been studied and compared with those of other First American Natives and worldwide populations (a total of 15694 chromosomes from 73 different populations were analyzed). This study corroborate the restricted HLA polymorphism in the Amerindian populations and demonstrate how the Amerindians show a relatively homogeneity as opposed to other First Native American groups. Finally, the present data support previous ones that state the lack of complete correlation between language and genetics in micro-environmental studies; Teenek Mayan language does not correspond with a close Mayan (Guatemala) relatedness.
Subject(s)
Chromosomes, Human/genetics , Histocompatibility Antigens Class II/genetics , Histocompatibility Antigens Class I/genetics , Indians, South American/genetics , Population/genetics , Alleles , Gene Frequency , Humans , Indians, South American/classification , PhylogenyABSTRACT
BACKGROUND AND AIMS: It has been postulated that the HFE C282Y mutation (linked to human leukocyte antigen [HLA]-A3-B7 haplotype) is not only responsible for hereditary hemochromatosis; HLA class I alleles would also contribute to the disease pathogenesis. In addition, H63D mutation linked to HLA-A29-B44 would also be pathogenetic, particularly in the Mediterranean Basin and throughout the world. However, sporadic porphyria cutanea tarda (s-PCT) has also been linked to these HFE mutations. In the present work, we have studied HFE mutations and HLA genes to test these hypotheses. METHODS: C282Y and H63D mutations together with HLA genetic typing have been performed in Spanish hereditary hemochromatosis (n = 98) and PCT (n = 63) patients. The etiologic fraction (delta) has been used to determine the absolute strongest gene linkage to both diseases. RESULTS: The Spanish frequent HLA-A29-B44 haplotype is not significantly associated to the H63D mutations in hereditary hemochromatosis patients (although it is found more frequently in patients than in controls). Sporadic porphyria cutanea tarda patients do not show a significant association to H63D mutations, although it is also more frequent than in controls; however, compound H63D/C282Y subjects seem to bear a significant risk to s-PCT. Allelic C282Y (and not H63D) frequencies show a significant association with s-PCT. CONCLUSIONS: The postulated additional risk of hereditary hemochromatosis given by class I HLA antigens may be secondary to the HFE gene linkage disequilibrium with certain class I alleles or to the existence of other neighboring genetic pathogenetic factors in our Spanish sample.
Subject(s)
HLA Antigens/genetics , Haplotypes/genetics , Hemosiderosis/genetics , Histocompatibility Antigens Class I/genetics , Membrane Proteins/genetics , Mutation , Porphyria Cutanea Tarda/genetics , Alleles , Antibodies, Monoclonal , DNA/genetics , Gene Frequency/genetics , Genetic Markers , HLA Antigens/immunology , Hemochromatosis Protein , Hemosiderosis/blood , Hemosiderosis/ethnology , Histocompatibility Antigens Class I/immunology , Humans , Membrane Proteins/immunology , Mutation/genetics , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Porphyria Cutanea Tarda/blood , Porphyria Cutanea Tarda/ethnology , Prevalence , Spain/epidemiologyABSTRACT
Two theories about MHC allele generation have been put forward: (1) point mutation diversification and/or (2) gene conversion events. A model supporting the existence of both of these mechanisms is shown in this paper; the possible evolution of the HLA-B*570101 and HLA-B*5801 alleles (which belong to the HLA-B17 serology group) is studied. The hypothesis favoured is that gene conversion events have originated these alleles, because intron sequences are also analysed. Evolution by point mutation should only be accepted if flanking introns have also been sequenced.
