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Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil

BACKGROUND: The present study sought to investigate the association between HLA-A, HLA-B and HLA-DRB1 genes and susceptibility or resistance to the different clinical manifestations of American cutaneous leishmaniasis (ACL) in southern Brazil. METHODS: The sample consisted of 169 patients with a dia...

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Autores principales: Ribas-Silva, Rejane C, Ribas, Adriana D, dos Santos, Maria CG, da Silva, Waldir V, Lonardoni, Maria VC, Borelli, Sueli D, Silveira, Thaís GV
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652734/
https://www.ncbi.nlm.nih.gov/pubmed/23638805
http://dx.doi.org/10.1186/1471-2334-13-198
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author Ribas-Silva, Rejane C
Ribas, Adriana D
dos Santos, Maria CG
da Silva, Waldir V
Lonardoni, Maria VC
Borelli, Sueli D
Silveira, Thaís GV
author_facet Ribas-Silva, Rejane C
Ribas, Adriana D
dos Santos, Maria CG
da Silva, Waldir V
Lonardoni, Maria VC
Borelli, Sueli D
Silveira, Thaís GV
author_sort Ribas-Silva, Rejane C
collection PubMed
description BACKGROUND: The present study sought to investigate the association between HLA-A, HLA-B and HLA-DRB1 genes and susceptibility or resistance to the different clinical manifestations of American cutaneous leishmaniasis (ACL) in southern Brazil. METHODS: The sample consisted of 169 patients with a diagnosis of ACL and 270 healthy subjects for comparison. HLA-A, HLA-B and HLA-DRB1 were typed by PCR-SSO reverse dot blot. RESULTS: Results showed a trend towards susceptibility to cutaneous lesions for alleles HLA-DRB1*13 (P=0.0228; Pc=0.3420; OR=1.66; 95%CI=1.08 – 2.56), HLA-B*35 (P=0.0218; Pc=0.6758; OR=1.67; 95%CI=1.08 – 2.29) and HLA-B*44 (P=0.0290; Pc=0.8990; OR=1.67; 95%CI=1.05 – 2.64). Subjects with allele HLA-B*27 (P=0.0180; Pc=0.5580; OR=7.1111; 95%CI=1.7850 – 28.3286) tended towards susceptibility to mucocutaneous lesions, those with HLA-B*49 (P=0.0101; Pc=0.3131; OR=6.4000; 95%CI=1.8472 – 22.1743) to recurrent ACL, and HLA-B*52 (P=0.0044; Pc=0.1360; OR=12.61; 95%CI=3.08 – 51.66), to re-infection. Presence of HLA-B*45 (P=0.0107; Pc=0.3317) tended to provide protection against the cutaneous form of ACL. The most frequent haplotypes that may be associated with susceptibility to ACL were A*02 B*44 DRB1*07 (P = 0.0236) and A*24 B*35 DRB1*01 (P = 0.0236). CONCLUSION: Some Class I and Class II HLA genes appear to contribute towards susceptibility to and protection against different clinical manifestations of ACL. Other genetic marker studies may contribute toward future prophylactic and therapeutic interventions in ACL.
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spelling pubmed-36527342013-05-14 Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil Ribas-Silva, Rejane C Ribas, Adriana D dos Santos, Maria CG da Silva, Waldir V Lonardoni, Maria VC Borelli, Sueli D Silveira, Thaís GV BMC Infect Dis Research Article BACKGROUND: The present study sought to investigate the association between HLA-A, HLA-B and HLA-DRB1 genes and susceptibility or resistance to the different clinical manifestations of American cutaneous leishmaniasis (ACL) in southern Brazil. METHODS: The sample consisted of 169 patients with a diagnosis of ACL and 270 healthy subjects for comparison. HLA-A, HLA-B and HLA-DRB1 were typed by PCR-SSO reverse dot blot. RESULTS: Results showed a trend towards susceptibility to cutaneous lesions for alleles HLA-DRB1*13 (P=0.0228; Pc=0.3420; OR=1.66; 95%CI=1.08 – 2.56), HLA-B*35 (P=0.0218; Pc=0.6758; OR=1.67; 95%CI=1.08 – 2.29) and HLA-B*44 (P=0.0290; Pc=0.8990; OR=1.67; 95%CI=1.05 – 2.64). Subjects with allele HLA-B*27 (P=0.0180; Pc=0.5580; OR=7.1111; 95%CI=1.7850 – 28.3286) tended towards susceptibility to mucocutaneous lesions, those with HLA-B*49 (P=0.0101; Pc=0.3131; OR=6.4000; 95%CI=1.8472 – 22.1743) to recurrent ACL, and HLA-B*52 (P=0.0044; Pc=0.1360; OR=12.61; 95%CI=3.08 – 51.66), to re-infection. Presence of HLA-B*45 (P=0.0107; Pc=0.3317) tended to provide protection against the cutaneous form of ACL. The most frequent haplotypes that may be associated with susceptibility to ACL were A*02 B*44 DRB1*07 (P = 0.0236) and A*24 B*35 DRB1*01 (P = 0.0236). CONCLUSION: Some Class I and Class II HLA genes appear to contribute towards susceptibility to and protection against different clinical manifestations of ACL. Other genetic marker studies may contribute toward future prophylactic and therapeutic interventions in ACL. BioMed Central 2013-05-02 /pmc/articles/PMC3652734/ /pubmed/23638805 http://dx.doi.org/10.1186/1471-2334-13-198 Text en Copyright © 2013 Ribas-Silva et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Ribas-Silva, Rejane C
Ribas, Adriana D
dos Santos, Maria CG
da Silva, Waldir V
Lonardoni, Maria VC
Borelli, Sueli D
Silveira, Thaís GV
Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil
title Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil
title_full Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil
title_fullStr Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil
title_full_unstemmed Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil
title_short Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil
title_sort association between hla genes and american cutaneous leishmaniasis in endemic regions of southern brazil
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652734/
https://www.ncbi.nlm.nih.gov/pubmed/23638805
http://dx.doi.org/10.1186/1471-2334-13-198
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