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This article is part of the supplement: 15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access Meeting abstract

Human leukocyte antigen (HLA) class I frequencies in human T-cell lymphotropic virus type 1 (HTLV-1)-infected patients from Salvador-Brazil

Viviana N Olavarria1, Maria F Grassi12, Ramon Kruschewsky1, Xiao-Jiang Gao3, Alline Nascimento1, David Watkins4, Mary Carrigton3 and Bernardo Galvao-Castro12*

Author Affiliations

1 Bahiana School of Medicine and Public Health (EBMSP) Salvador, Bahia, Brazil

2 Advanced Laboratory of Public Health, Gonçalo Moniz Center, Fundação Oswaldo Cruz, Salvador, Bahia, Brazil

3 Laboratory of Genomic Diversity, SAIC-Frederick, Inc., National Cancer Institute, Frederick, Maryland, 21702, USA

4 Wisconsin National Primate Center, University of Wisconsin–Madison, Madison, Wisconsin, USA

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Retrovirology 2011, 8(Suppl 1):A121  doi:10.1186/1742-4690-8-S1-A121


The electronic version of this article is the complete one and can be found online at: http://www.retrovirology.com/content/8/S1/A121


Published:6 June 2011

© 2011 Olavarria et al; licensee 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.

Introduction

The development of human T- cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) may be related to genetic factors related to the presentation of viral antigens by human leukocyte antigen (HLA).

Aim

To determine the HLA class I genotype of HTLV-1-infected patients.

Methods

420 HTLV-1-infected patients (280 healthy carriers (HC) and 140 HAM/TSP) from the HTLV Reference Center in Salvador, Brazil were evaluated. HLA genotype was performed using automated DNA sequencers and analyzed using the software program Assign-SBT TM 3.2.

Results

The HLA types most frequently observed in all individuals combined were A*02 (26.1%), A*03 (10.5%); B*35 (13.1%), B*44 (10.4%), Cw*04 (21.9) and Cw* 07 (17.7%). The presence of HLA-A*02 reduced the odds of HAM-TSP (Odds Ratio: 0.4, p<0.0001 and IC95%: 0.28-0.59). The frequency of homozygosity of HLA-A was 8%, 4% for HLA-B and 9% for HLA-C overall. Proviral load was significantly lower in HC among those heterozygous at all three HLA class I loci group relative to HC who were homozygous at one or more HLA class I loci group (p = 0.029). However, no difference in homozygosity between proviral load in the HAM/TSP patients was observed (p = 0.57).

Conclusion

HLA-A*02 allele is more prevalent in the HC patients, which suggests a protective role of this allele against HAM/TSP. Furthermore, HC patients had a higher frequency of heterozygosity at all three HLA class than that in HAM/TSP patients.