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  • Oral presentation
  • Open Access

Humoral immune response to HTLV-1 basic leucine zipper factor (HBZ) in HTLV-1-infected individuals

  • 1,
  • 1,
  • 1,
  • 2,
  • 3,
  • 4,
  • 5, 6 and
  • 1Email author
Retrovirology201411 (Suppl 1) :O23

https://doi.org/10.1186/1742-4690-11-S1-O23

  • Published:

Keywords

  • Antibody Response
  • Virus Type
  • Humoral Immune Response
  • Asymptomatic Carrier
  • Proviral Load

Human T cell lymphotropic virus type I (HTLV-I) infection can lead to development of adult T cell leukemia/lymphoma (ATL) or HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in a subset of infected subjects. HTLV-I basic leucine zipper factor (HBZ) gene has a critical role in HTLV-I infectivity and the development of ATL and HAM/TSP. However, little is known about immune response against HBZ in HTLV-I-infected individuals. In this study, we examined antibody responses against HBZ in serum/plasma samples from 436 subjects including HTLV-I seronegative donors, asymptomatic carriers (AC), ATL, and HAM/TSP patients by the luciferase immunoprecipitation system. The immunoreactivity for HBZ was detected in subsets of all HTLV-I-infected individuals but did not discriminate between AC, ATL and HAM/TSP. However, the frequency of detection of HBZ-specific antibodies in the serum of ATL patients with the chronic subtype was higher than in ATL patients with the lymphomatous subtype. Antibody responses against HBZ were also detected in CSF of HAM/TSP patients with anti-HBZ in serum. Antibody responses against HBZ did not correlate with proviral load and HBZ mRNA expression in HAM/TSP patients, but the presence of HBZ-specific response was associated with reduced CD4+ T cell activation in HAM/TSP patients. Moreover, HBZ-specific antibody inhibited lymphoproliferation in PBMC of HAM/TSP patients. This is the first report demonstrating humoral immune response against HBZ associated with HTLV-I infection. Thus, humoral immune response against HBZ might play a role in HTLV-I infection.

Authors’ Affiliations

(1)
Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
(2)
Department of General and Experimental Pathology, Medical University of Bialystok, Bialystok, Poland
(3)
Bioinformatics Section, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
(4)
Center for Retrovirus Research, The Ohio State University, Columbus, OH, USA
(5)
Formerly of the Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
(6)
Present address: Center for Drug Evaluation and Research, Office of Surveillance and Epidemiology, Food and Drug Administration, Silver Spring, MD, USA

Copyright

© Enose-Akahata 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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