Volume 11 Supplement 1

16th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

Correlation of increased CXCL13 with intrathecal humoral immune responses to HTLV-1 in CSF of patients with HAM/TSP

  • Yoshimi Enose-Akahata1,
  • Raya Massoud1,
  • Jussi O Virtanen1 and
  • Steven Jacobson1Email author
Retrovirology201411(Suppl 1):O38

https://doi.org/10.1186/1742-4690-11-S1-O38

Published: 7 January 2014

Intrathecal antibody synthesis is a well-documented phenomenon in infectious neurological diseases as well as in demyelinating diseases. Intrathecal antibody synthesis against HTLV-1 has been reported in HAM/TSP, but little is known about the role of B cells and humoral immune responses in the central nervous systems (CNS) of HAM/TSP patients. Here we demonstrate profiles of HTLV-1-specific antibodies in cerebrospinal fluid (CSF) of HAM/TSP patients. Of 36 HAM/TSP patients, antibody responses against Gag and Tax were detected in CSF of all the patients. CSF/Serum antibody ratio was elevated in anti-Gag (mean 1.20) more than in anti-Tax (mean 0.85), but importantly HAM/TSP patients with lesions or atrophy in spinal cord showed higher CSF/Serum anti-Gag antibody ratio. Antibody response against Env was detected in CSF of 94.4% of patients, but CSF/serum anti-Env ratio was significantly lower than those of anti-Gag and anti-Tax (mean 0.18). 19 patients were further studied for oligoclonal band (OCB) specificity to HTLV-1 antigens and all of them were found to have bands specific for at least one antigen studied. Significantly higher proportion of patients had Gag- or Env-specific OCBs than Tax-specific OCBs. Interestingly, CXCL13 (B cell attracting chemokine-1) was increased in CSF of HAM/TSP patients, which was associated with higher HTLV-1-specific antibody responses in CSF and was correlated with decrease of plasma blasts in peripheral blood. These results highlight the importance of the B cell compartment in HAM/TSP where production of HTLV-1-specific antibody may be required to control viral persistence and/or may be associated with HAM/TSP disease progression.

Authors’ Affiliations

(1)
Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health

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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