dc.creatorLopes M.P.
dc.creatorSantos M.N.N.
dc.creatorFaber E.W.
dc.creatorBezerra M.A.C.
dc.creatorHatzlhofer B.L.D.
dc.creatorAlbuquerque D.M.
dc.creatorZaccariotto T.R.
dc.creatorRibeiro D.M.
dc.creatorDa Silva Araujo A.
dc.creatorCosta F.F.
dc.creatorDe Fatima Sonati M.
dc.date2014
dc.date2015-06-25T18:03:07Z
dc.date2015-11-26T15:05:21Z
dc.date2015-06-25T18:03:07Z
dc.date2015-11-26T15:05:21Z
dc.date.accessioned2018-03-28T22:16:09Z
dc.date.available2018-03-28T22:16:09Z
dc.identifier
dc.identifierDisease Markers. Hindawi Publishing Corporation, v. 2014, n. , p. - , 2014.
dc.identifier2780240
dc.identifier10.1155/2014/678246
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84918769756&partnerID=40&md5=bde7ac5a854eee99659c2ca3ec05a486
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/87982
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/87982
dc.identifier2-s2.0-84918769756
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1257059
dc.descriptionBackground. Previous studies on the role of inflammation in the pathophysiology of sickle cell disease (SCD) suggested that the CCR5Δ32 allele, which is responsible for the production of truncated C-C chemokine receptor type 5 (CCR5), could confer a selective advantage on patients with SCD because it leads to a less efficient Th1 response. We determined the frequency of the CCR5Δ32 polymorphism in 795 Afro-Brazilian SCD patients followed up at the Pernambuco Hematology and Hemotherapy Center, in Northeastern Brazil, divided into a pediatric group (3 months-17 years, n = 483) and an adult group (18-70 years, n = 312). The adult patients were also compared to a healthy control group (blood donors, 18-61 years, n = 247). Methods. The CCR5/CCR5Δ32 polymorphism was determined by allele-specific PCR. Results. No homozygous patient for the CCR5Δ32 allele was detected. The frequency of heterozygotes in the study population (patients and controls) was 5.8%, in the total SCD patients 5.1%, in the children 5.4%, in the adults with SCD 4.8%, and in the adult controls 8.1%. These differences did not reach statistical significance. Conclusions. Our findings failed to demonstrate an important role of the CCR5Δ32 allele in the population sample studied here.
dc.description2014
dc.description
dc.description
dc.description
dc.descriptionSteinberg, M.H., Pathophysiologically based drug treatment of sickle cell disease (2006) Trends in Pharmacological Sciences, 27 (4), pp. 204-210
dc.descriptionSteinberg, M.H., Sickle cell anemia, the firstmolecular disease: Overviewofmolecular etiology, pathophysiology, and therapeutic approaches (2008) The Scientific World Journal, 8, pp. 1295-1324
dc.descriptionMarotta, C.A., Wilson, J.T., Forget, B.J., Weissman, S.M., Human β globin messenger RNA III. Nucleotide sequences derived from complementary DNA (1977) The Journal of Biological Chemistry, 252 (14), pp. 5040-5053
dc.descriptionSteinberg, M.H., Brugnara, C., Pathophysiological-based approaches to treatment of sickle cell disease (2003) Annual Review of Medicine, 54, pp. 89-112
dc.descriptionDe Sonati, M.F., Costa, F.F., The genetics of blood disorders: Hereditary hemoglobinopathies (2008) Jornal de Pediatria, 84 (4), pp. S40-S51
dc.descriptionZago, M.A., Pinto, A.C.S., The pathophysiology of sickle cell disease: From the genetic mutation to multiorgan disfunction (2007) Revista Brasileira de Hematologia e Hemoterapia, 29 (3), pp. 207-214
dc.descriptionEmbury, S.H., The not-so-simple process of sickle cell vasoocclusion (2004) Microcirculation, 11 (2), pp. 101-113
dc.descriptionRees, D.C., Williams, T.N., Gladwin, M.T., Sickle-cell disease (2010) The Lancet, 376 (9757), pp. 2018-2031
dc.descriptionKutlar, A., Sickle cell disease: A multigenic perspective of a single-gene disorder (2005) Medical Principles and Practice, 14, pp. 15-19
dc.descriptionChies, J.A.B., Nardi, N.B., Sickle cell disease: A chronic inflammatory condition (2001) Medical Hypotheses, 57 (1), pp. 46-50
dc.descriptionHebbel, R.P., Osarogiagbon, R., Kaul, D., The endothelial biology of sickle cell disease: Inflammation and a chronic vasculopathy (2004) Microcirculation, 11 (2), pp. 129-151
dc.descriptionVargas, A.E., Marrero, A.R., Salzano, F.M., Bortolini, M.C., Chies, J.A.B., Frequency of CCR5Δ32 in Brazilian populations (2006) Brazilian Journal of Medical and Biological Research, 39 (3), pp. 321-325
dc.descriptionLiu, R., Paxton, W.A., Choe, S., Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection (1996) Cell, 86 (3), pp. 367-377
dc.descriptionBenkirane, M., Jin, D.-Y., Chun, R.F., Koup, R.A., Jeang, K.-T., Mechanism of transdominant inhibition of CCR5-mediated HIV-1 infection by ccr5Δ32 (1997) The Journal of Biological Chemistry, 272 (49), pp. 30603-30606
dc.descriptionChies, J.A.B., Hutz, M.H., High frequency of the CCR5delta32 variant among individuals from an admixed Brazilian population with sickle cell anemia (2003) Brazilian Journal of Medical and Biological Research, 36 (1), pp. 71-75
dc.descriptionLidén, K., Linderholm, A., Götherström, A., Pushing it back. Dating the CCR5-D32 bp deletion to the Mesolithic in Sweden and its implications for the Meso/Neo transition (2006) Documenta Praehistorica, 33, pp. 29-37
dc.descriptionSamson, M., Libert, F., Doranz, B.J., Resistance to HIV-1 infection in caucasian individuals bearing mutant alleles of the CCR-5 chemokine receptor gene (1996) Nature, 382 (6593), pp. 722-726
dc.descriptionLibert, F., Cochaux, P., Beckman, G., The Δccr5 mutation conferring protection against HIV-1 in Caucasian populations has a single and recent origin in Northeastern Europe (1998) Human Molecular Genetics, 7 (3), pp. 399-406
dc.descriptionLucotte, G., Frequencies of 32 base pair deletion of the (Δ32) allele of the CCR5 HIV-1 co-receptor gene in Caucasians: A comparative analysis (2002) Infection, Genetics and Evolution, 1 (3), pp. 201-205
dc.descriptionGalvani, A.P., Novembre, J., The evolutionary history of the CCR5-Delta32 HIV-resistance mutation (2005) Microbes and Infection, 7 (2), pp. 302-309
dc.descriptionVargas, A.E., Cechim, G., Correa, J.F., Pros and cons of a missing chemokine receptor-Comments on "Is the European spatial distribution of the HIV-1-resistant CCR5-Δ32 allele formed by a breakdown of the pathocenosis due to the historical Roman expansion?" by Eric Faure and Manuela Royer-Carenzi (2008) (2009) Infection, Genetics and Evolution, 9 (4), pp. 387-389
dc.descriptionFaure, E., Royer-Carenzi, M., Is the European spatial distribution of the HIV-1-resistant CCR5-Δ32 allele formed by a breakdown of the pathocenosis due to the historical Roman expansion? (2008) Infection, Genetics and Evolution, 8 (6), pp. 864-874
dc.descriptionMartinson, J.J., Chapman, N.H., Rees, D.C., Liu, Y.-T., Clegg, J.B., Global distribution of the CCR5 gene 32-basepair deletion (1997) Nature Genetics, 16 (1), pp. 100-103
dc.descriptionCarvalhaes, F.A.D.P.L., Cardoso, G.L., Hamoy, I.G., Yan, T.L., Guerreiro, J.F., Distribution of CCR5-Δ32, CCR2-64I, and SDF1-3′A mutations in populations from the Brazilian Amazon region (2004) Human Biology, 76 (4), pp. 643-646
dc.descriptionCarvalho, M.W.P., Leboute, A.P.M., Oliveira, S.F., Sousa, S.M.B., De Nazaré Klautau-Guimarães, M., Simões, A.L., CCR5D32 mutation in three Brazilian populations of predominantly Sub-Saharan African ancestry (2004) Genetics and Molecular Biology, 27 (3), pp. 321-325
dc.descriptionBoldt, A.B.W., Culpi, L., Tsuneto, L.T., Souza, I.R., Kun, J.F.J., Petzl-Erler, M.L., Analysis of the CCR5 gene coding region diversity in five South American populations reveals two new non-synonymous alleles in Amerindians and high CCR5∗D32 frequency in Euro-Brazilians (2009) Genetics and Molecular Biology, 32 (1), pp. 12-19
dc.descriptionTeixeira, S.L.M., Bastos, F.I., Hacker, M.A., Morgado, M.G., Distribution of CCR5 genotypes and HLA Class I B alleles in HIV-1 infected and uninfected injecting drug users from Rio de Janeiro, Brazil (2009) Infection, Genetics and Evolution, 9 (4), pp. 638-642
dc.descriptionVieira, V.C., Barral, M.F.M., Mendoza-Sassi, R.A., Silveira, J.M., Soares, M.A., De Martínez, A.M.B., The effect of combined polymorphisms in chemokines and chemokine receptors on the clinical course of HIV-1 infection in a Brazilian population (2011) Memórias Do Instituto Oswaldo Cruz, 106 (4), pp. 408-415
dc.descriptionGrimaldi, R., Shindo, N., Acosta, A.X., Prevalence of the CCR5Δ32 mutation in Brazilian populations and cell susceptibility to HIV-1 infection (2002) Human Genetics, 111 (1), pp. 102-104
dc.descriptionRigato, P.O., Hong, M.A., Casseb, J., Better CD4+ T cell recovery in Brazilian HIV-infected individuals under HAART due to commulative carriage of SDF-1-3′ A, CCR2-V64I, CCR5-D32 and CCR5-promoter 59029A/G Polymorphisms (2008) Current HIV Research, 6 (5), pp. 466-473
dc.descriptionHünemeier, T., Neves, A.G., Nornberg, I., T-cell and chemokine receptor variation in South Amerindian populations (2005) American Journal of Human Biology, 17 (4), pp. 515-518
dc.descriptionDe Farias, J.D., Santos, M.G., De Franc¸a, A.K., Distribution of the CCR5delta32 allele (gene variant CCR5) in Rondônia, Western Amazonian region, Brazil (2012) Genetics and Molecular Biology, 35 (1), pp. 27-31
dc.descriptionJones, K.L., Maguire, J.J., Davenport, A.P., Chemokine receptor CCR5: From AIDS to atherosclerosis (2011) British Journal of Pharmacology, 162 (7), pp. 1453-1469
dc.descriptionPichenot, M., Deuffic-Burban, S., Cuzin, L., Yazdanpanah, Y., Efficacy of new antiretroviral drugs in treatment-experienced HIV-infected patients: A systematic review and meta-analysis of recent randomized controlled trials (2012) HIV Medicine, 13 (3), pp. 148-155
dc.descriptionDorr, P., Westby, M., Dobbs, S., Maraviroc (UK-427,857), a potent, orally bioavailable, and selective small-molecule inhibitor of chemokine receptor CCR5 with broad-spectrum anti-human immunodeficiency virus type 1 activity (2005) Antimicrobial Agents and Chemotherapy, 49 (11), pp. 4721-4732
dc.descriptionKaraali, Z.E., Sozen, S., Yurdum, M., Effect of genetic variants of chemokine receptors on the development of myocardial infarction in Turkish population (2010) Molecular Biology Reports, 37 (7), pp. 3615-3619
dc.descriptionZhao, Q., Dual targeting of CCR2 and CCR5: Therapeutic potential for immunologic and cardiovascular diseases (2010) Journal of Leukocyte Biology, 88 (1), pp. 41-55
dc.descriptionZapico, I., Coto, E., Rodríguez, A., Alvarez, C., Torre, J.C., Alvarez, V., CCR5 (chemokine receptor-5) DNA-polymorphism influences the severity of rheumatoid arthritis (2000) Genes & Immunity, 1 (4), pp. 288-289
dc.descriptionZúñiga, J.A., Villareal-Garza, C., Flores, E., Biological relevance of the polymorphism in the CCR5 gene in refractory and non-refractory rheumatoid arthritis in Mexicans (2003) Clinical and Experimental Rheumatology, 21 (3), pp. 351-354
dc.descriptionPetrek, M., Cermáková, Z., Hutyrová, B., CC chemokine receptor 5 and interleukin-1 receptor antagonist gene polymorphisms in patients with primary Sjögren's syndrome (2002) Clinical and Experimental Rheumatology, 20 (5), pp. 701-703
dc.descriptionSrivastava, P., Helms, P.J., Stewart, D., Main, M., Russell, G., Association of CCR5δ32 with reduced risk of childhood but not adult asthma (2003) Thorax, 58 (3), pp. 222-226
dc.descriptionVargas, A.E., Da Silva, M.A.L., Silla, L., Chies, J.A.B., Polymorphisms of chemokine receptors and eNOS in Brazilian patients with sickle cell disease (2005) Tissue Antigens, 66 (6), pp. 683-690
dc.languageen
dc.publisherHindawi Publishing Corporation
dc.relationDisease Markers
dc.rightsfechado
dc.sourceScopus
dc.titleThe Ccr5Δ32 Polymorphism In Brazilian Patients With Sickle Cell Disease
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución