Volume 2 Issue 4
Dec.  2018
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Sepúlveda-Delgado J, Danis-Lozano R, Ocaa-Sibilla MJ, Ramirez-Valdespino JC, Cetina-Díaz JH, Bulos-Rodriguez P, Hernández-Doo S, Ruiz-Gómez D, García R, Juárez-Nicolás F, Tevera-Gamboa MG, Vera-Lastra OL, Jara LJ, Canseco-Avila LM, Dominguez-Arrevillaga S, Trujillo-Murillo K, Julio Granados J. Role of HLA DRB1*15 and HLA DRB1*16alleles in the genetic susceptibility to develop systemic lupus erythematosus (SLE) after Chikungunya and Zika viruses infection in México[J]. Blood&Genomics, 2018, 2(4): 233-236. doi: 10.46701/APJBG.2018042018127
Citation: Sepúlveda-Delgado J, Danis-Lozano R, Ocaa-Sibilla MJ, Ramirez-Valdespino JC, Cetina-Díaz JH, Bulos-Rodriguez P, Hernández-Doo S, Ruiz-Gómez D, García R, Juárez-Nicolás F, Tevera-Gamboa MG, Vera-Lastra OL, Jara LJ, Canseco-Avila LM, Dominguez-Arrevillaga S, Trujillo-Murillo K, Julio Granados J. Role of HLA DRB1*15 and HLA DRB1*16alleles in the genetic susceptibility to develop systemic lupus erythematosus (SLE) after Chikungunya and Zika viruses infection in México[J]. Blood&Genomics, 2018, 2(4): 233-236. doi: 10.46701/APJBG.2018042018127

Role of HLA DRB1*15 and HLA DRB1*16alleles in the genetic susceptibility to develop systemic lupus erythematosus (SLE) after Chikungunya and Zika viruses infection in México

doi: 10.46701/APJBG.2018042018127
  • Publish Date: 2018-12-30
  • Systemic lupus erythematosus (SLE) is a clinically and genetically heterogeneous disease particularly prevalent in Mexico. Althoughits etiology is unknown, genetic factors strongly influence its presenceas well as triggering factors, such as viral infections, including Cytomegalovirus and Epstein-Barr virus. Here,the study presents the appearance of de novoSLE (patients who did not present SLE before de virus infection, corroborated by serological analysis and negative for antinuclear antibodies) cases in Mexicans who live near the southern border of Mexico, who presented clinical symptoms of arthritic, hematological, mucocutaneous and renal SLE, after Zika and/ or Chikungunya virus infection. Low resolution class Ⅱ HLA typing was performed, which found a significantly increased frequency of HLA DRB1*02 (15 and 16)when compared to a group of 99 healthy individuals (P =0.001, OR=4.5, IC95% 1.8~11.0). All the patients were diagnosed with SLE 1 to 3 years after being confirmed with the Zika, and/or Chikungunya infection. At the point of acute viral infection, none of the patients presented clinical signs or symptoms of autoimmunity or were negative for antinuclear antibodies. In genetically susceptible individuals, Zika and Chikungunya viral infection can trigger SLE.

     

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