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1.
AIDS Res Hum Retroviruses ; 13(12): 987-93, 1997 Aug 10.
Artículo en Inglés | MEDLINE | ID: mdl-9264285

RESUMEN

We developed and evaluated two peptide-based immunoassays to confirm and discriminate between group M and group O HIV-1 infection. These assays are based on in vitro competition for antibody binding between M and O peptides. The first EIA is based on competition between group M and group O gp41 immunodominant domains and the second on competition between group O and group M V3 regions of gp120. Two panels of sera were used: the first consisted of 109 sera collected from 27 group O- and 92 group M-infected patients in whom the HIV isolates had been genotyped by sequencing or heteroduplex mobility assay. In this panel, the combination of the two assays correctly discriminated 106 samples (100% group O and 96.7% group M samples). The second panel, used for the field evaluation of the two assays, consisted of 157 samples from HIV-1-infected Cameroonian patients, 33 strains having been genotyped. The combination of the two techniques in a serogrouping algorithm discriminated 147 of these samples, 74 being HIV-1 group O and 73 group M. These results always correlated with genotyping results. The 10 sera that were not successfully classified by these assays were from early seroconverters. Altogether, the two assays clearly differentiated 263 of 276 (94.9%) samples in the two panels. On the basis of the genotyping results, the positive predictive value for group discrimination in the two panels was 100% for both GSEIA assays. Our peptide-blocking group-specific EIAs for differentiation and confirmation of HIV-1 group M and group O infection are complementary tools for epidemiological studies and surveillance of HIV-1 group O strain trafficking.


Asunto(s)
Ensayo de Inmunoadsorción Enzimática/métodos , Infecciones por VIH/virología , VIH-1/clasificación , Secuencia de Aminoácidos , Antígenos VIH/inmunología , Proteína gp120 de Envoltorio del VIH/inmunología , Proteína gp41 de Envoltorio del VIH/inmunología , Infecciones por VIH/sangre , Infecciones por VIH/inmunología , VIH-1/inmunología , Humanos , Epítopos Inmunodominantes/inmunología , Datos de Secuencia Molecular , Fragmentos de Péptidos/inmunología , Péptidos/síntesis química , Péptidos/inmunología , Sensibilidad y Especificidad , Serotipificación
2.
Hum Genet ; 89(3): 333-7, 1992 May.
Artículo en Inglés | MEDLINE | ID: mdl-1376298

RESUMEN

The sickle cell mutation (beta s) arose as at least three independent events in Africa and once in Asia, being termed the Senegal, Benin, Bantu and Indian types respectively. An investigation in Cameroon was carried out to determine whether the atypical sickle genes observed in the neighboring countries are the result of recombination or the presence of a sickle cell mutation of a different genetic origin. It was conducted on 40 homozygous SS patients followed at the Blood Transfusion Center in the capital city of Yaoundé. On 80 beta s chromosomes, 13 exhibited a novel polymorphic pattern that was observed three times in the homozygous state. This chromosome contains an A gamma T gene. The restriction fragment length polymorphism haplotype is different from all the other beta s chromosomes in both the 5' and 3' regions, but has previously been reported in sporadic cases. The (AT)8(T)5 sequence in the -500 region of the beta gene is specific and different from that of the Senegal, Benin, Bantu or Indian beta s genes. All the carriers of this specific chromosome belong to the Eton ethnic group and originate from the Sanaga river valley. This observation strongly argues for yet another independent origin of the sickle cell mutation in Africa, here referred to as the "Cameroon type". The Benin haplotype and a Benin/Bantu recombinant haplotype have been observed in the other studied populations: Ewondo, Bamiléké, Bassa, Yambassa and Boulou.


Asunto(s)
Anemia de Células Falciformes/genética , Hemoglobina Falciforme/genética , Polimorfismo de Longitud del Fragmento de Restricción , Secuencia de Bases , Southern Blotting , Camerún , Hemoglobina Fetal , Humanos , Desequilibrio de Ligamiento , Datos de Secuencia Molecular , Mutación/genética , Reacción en Cadena de la Polimerasa , Recombinación Genética/genética
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