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  • Open Access

HLA-G 3142C/G polymorphism is related to development of symptoms in HTLV-1 infected individuals

  • 1,
  • 2, 3Email author,
  • 4,
  • 2,
  • 1,
  • 1, 2,
  • 2, 3 and
  • 1
Retrovirology201411 (Suppl 1) :P74

https://doi.org/10.1186/1742-4690-11-S1-P74

  • Published:

Keywords

  • Human Leukocyte
  • 3142GG Genotype
  • Related Disease
  • Immunosuppressive Effect
  • Proviral Load

The majority of HTLV-1 infected individuals remain asymptomatic (HAC) throughout life, and the risk factors associated to the development of related diseases, such as HAM/TSP and ATL, are not fully understood. The human leukocyte antigen-G (HLA-G) is expressed in several pathological conditions and it has been associated to immunosuppressive effects allowing the virus-infected cells to escape of the host antiviral defense. Here, we evaluated the correlation between HLA-G polymorphisms in symptomatic and asymptomatic HTLV-1 infected individuals. Four polymorphisms of the exon 8 of the HLA-G gene were analysed by gene sequencing in HAC (n=48) and HAM/TSP patients (n=43). No difference was found between the groups for 3035C/T, 3187A/G and 3196C/G polymorphisms. On the other hand, despite of the absence of statistical significance, HAC group showed higher frequency of the 3142GG genotype (responsible for decreased transcription of theHLA-G) compared to HAM/TSP group (p=0,0607). Still, HAC group showed lower frequency of the 3142CC genotype (responsible for increased transcription of the HLA-G) compared to HAM/TSP group (p=0,0762). Furthermore, HAC group showed statistically higher frequency of the 3142G allele and lower frequency of the 3142C allele compared to HAM/TSP group (p=0,0244). In conclusion, HTLV-1-related symptoms in HAM/TSP group could be partially determined by higher expression of HLA-G (caused by higher frequency of the 3142C allele). We hypothesise that the higher expression of HLA-G protects the HTLV-1 infected cell against immune system attack the increasing proviral load and trigger the HAM/TSP symptoms.

Financial support

FUNDHERP, FAPESP and CNPq.

Authors’ Affiliations

(1)
Faculdade de Medicina de Ribeirão Preto – USP, Ribeirão Preto, São Paulo, Brazil
(2)
Fundação Hemocentro de Ribeirão Preto, Ribeirão Preto, São Paulo, Brazil
(3)
Faculdade de Ciências Farmacêuticas de Ribeirão Preto – USP, Ribeirão Preto, São Paulo, Brazil
(4)
Faculdade de Ceilândia – UNB/FCE, Universidade de Brasília, Brasília, Distrito Federal, Brazil

Copyright

© Cilião-Alves et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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