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

Open Access Open Badges Meeting abstract

Does helminthic infection alter the clinical course of HTLV-1 infection?

Michael A Sundberg1*, Marshall J Glesby2 and Edgar M Carvalho3

Author Affiliations

1 Stanford University School of Medicine, Stanford, CA, 94305, USA

2 Weill Cornell Medical College, New York, NY, 10065, USA

3 Serviço de Imunologia, Hospital Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, BA, Brazil

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Retrovirology 2011, 8(Suppl 1):A47  doi:10.1186/1742-4690-8-S1-A47

The electronic version of this article is the complete one and can be found online at:

Published:6 June 2011

© 2011 Sundberg et al; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


HTLV-1 is associated with the development of HAM/TSP and overactive bladder (OB). A higher prevalence of helminthic coinfection has been observed among those infected with HTLV-1. Because helminthic infection may modify the immune response and influence clinical outcomes in HTLV-1 infection, we investigated the development of HAM/TSP and OB in HTLV-1 positive individuals with and without helminthic coinfection.


HTLV-1 patients enrolled in a cohort study between 2004-2010 were classified as coinfected and non-coinfected based on stool samples. All patients were followed at least two years from initial evaluation, with yearly clinical assessments. Disease-free survival for OB was estimated using the Kaplan-Meier method, and the relationship between helminthic infection and development of OB was assessed by Cox proportional hazard modeling.


Seventy-four coinfected and 79 non-coinfected patients were followed. A total of 92 helminthic infections were observed in the coinfected group. One patient from each group developed HAM/TSP during followup. Fourteen and 17 patients developed OB from the coinfected and non-coinfected groups, respectively. There was no association between helminthic infection and risk of OB (hazard ratio 0.91, 95% CI 0.43-1.89, p = 0.79, adjusted for sex).


We found no difference in the risk of development of OB in HTLV-1 and helminthic coinfected and non-coinfected patients. The incidence of HAM/TSP was low in each group. These data indicate that general helminthic infection does not modify development of HAM/TSP or OB. Future studies should address the potential association between specific helminthic infections and risk of neurologic disease in HTLV-1 infection.