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Open Access

Telomere length, proviral load and neurologic impairment in HTLV-1-and HTLV-2-infected humans

  • Benjamin Usadi1, 2,
  • Roberta Bruhn1,
  • Jue Lin3,
  • Tzong-Hae Lee1,
  • Elizabeth Blackburn3 and
  • Edward L Murphy3, 1
Retrovirology201411(Suppl 1):O15

https://doi.org/10.1186/1742-4690-11-S1-O15

Published: 7 January 2014

Keywords

NeuropathyInverse AssociationTelomere LengthNeurologic ImpairmentWeak Association

Background

Telomeres shorten with aging and short or damaged telomeres have been implicated in degenerative conditions. We hypothesized that telomere length might be altered in chronic HTLV-1 and -2 infection and could be a marker of HTLV-associated disease and viral dynamics.

Methods

45 HTLV-1, 45 HTLV-2, and 45 seronegative subjects were selected from the larger HTLV Outcomes Study (HOST) cohort, and stratum-matched on age, sex and race/ethnicity. The telomere-to-single copy gene (T/S) ratio and HTLV-1 and -2 proviral load were measured using real-time PCR on the same PBMC samples. Unpaired t-tests, linear regression and logistic regression were used to test associations.

Results

Ln T/S ratio was inversely associated with age among seronegatives (p=.006) but HTLV-1 and -2 subjects did not show an inverse age association. There was no difference in mean T/S ratio between HTLV-1 (1.02), HTLV-2 (1.03) and matched seronegative (0.99) subjects. In HTLV-1 subjects, there was a borderline inverse association (p=0.07) between T/S ratio and log10 proviral load which did not persist after multivariate adjustment (p=0.17). Among HTLV-2 subjects only, Ln T/S ratio was significantly associated (p=0.026) with increased odds of vibration-sensation impairment.

Conclusions

We found no evidence for an overall difference in telomere length between HTLV cases and controls but there was a weak association between HTLV-1 proviral load and telomere length. The association between telomere length and impaired vibration sense in the HTLV-2-positive group is intriguing, and suggests avenues for future investigation of previously described neuropathy in that group.

Authors’ Affiliations

(1)
Blood Systems Research Institute, San Francisco, USA
(2)
University of California, Berkeley, Berkeley, USA
(3)
University of California San Francisco, San Francisco, USA

Copyright

© Usadi 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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