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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

Clinical subtype of HAM/TSP based on clinical course and laboratory findings

Yoshihisa Yamano1*, Tomoo Sato1, Natsumi Araya1, Naoko Yagishita1, Yukiko Shimizu1, Hitoshi Ando1, Atae Utsunomiya2, Shuji Izumo3, Steven Jacobson4 and Noboru Suzuki1

Author Affiliations

1 Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan

2 Department of Hematology, Imamura Bun-in Hospital, Kagoshima, Japan

3 Molecular Pathology, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan

4 Viral Immunology Section, Neuroimmunology Branch, National Institute of Health, Bethesda, MD, USA

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Retrovirology 2011, 8(Suppl 1):A42  doi:10.1186/1742-4690-8-S1-A42

The electronic version of this article is the complete one and can be found online at: http://www.retrovirology.com/content/8/S1/A42


Published:6 June 2011

© 2011 Yamano 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.

Meeting abstract

The clinical course and disease activity of patients with HTLV-1 associated myelopathy / tropical spastic paraparesis (HAM/TSP) are different among patients. Therefore, the treatment plan should be designed based on these backgrounds of patients. However, there is little information about the natural history of HAM/TSP and biomarkers of disease activity that is associated with prognosis.

As the candidate for biomarkers to evaluate the disease activity in HAM/TSP, HTLV-1 proviral load in PBMC, several cytokines and chemokines in serum or cerebrospinal fluid (CSF) are known to be increased in HAM/TSP patients. However, little is known which parameter of these candidates is most associated with disease severity.

Therefore, we investigated the clinical course of 30 HAM/TSP patients without any history of treatment. Furthermore, we measured quantitatively the concentration of a series of cytokines and chemokines in serum and CSF, and HTLV-1 proviral DNA load in PBMC. Then, the level of these markers was evaluated for the correlation with disease severity.

In HAM/TSP patients, the level of CXCL10/IP-10 and neopterin in CSF was strongly correlated with disease severity. Interestingly, the level of soluble IL-2 receptor and CXCL10/IP-10 in serum was also correlated with disease severity with statistical significance. Furthermore, based on the clinical course and laboratory findings, HAM/TSP was classified into 4 different clinical subtypes as follows; (1) Rapidly progressive (active), (2-A) Chronic progressive (active), (2-B) Chronic progressive (inactive), (3) Chronic mild (inactive). This classification might be useful to determine the therapeutic strategy for patients with HAM/TSP.