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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

HTLV-1 proviral load levels in adult T-cell leukemia/lymphoma (ATL) in Bahia, Brazil

Isabela Archanjo1, Marcelo Magalhães1, Everton S Batista1, Kiyoshi Fukutani2, Achilea Bittencourt3 and Lourdes Farre1*

Author Affiliations

1 Laboratory of Experimental Pathology, CPQGM, FIOCRUZ, Salvador, Bahia, 40296710, Brazil

2 Laboratory of Immunoparasitology, CPQGM, FIOCRUZ, Salvador, Bahia, 40296710, Brazil

3 Department of Pathology, HUPES, Federal University of Bahia, Salvador, Bahia, 40296710, Brazil

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Retrovirology 2011, 8(Suppl 1):A91  doi:10.1186/1742-4690-8-S1-A91

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

Published:6 June 2011

© 2011 Archanjo 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.

Meeting abstract

In human T-cell leukemia virus type 1 (HTLV-1) infection, high levels of proviral load (PVL) have been associated with the development of HTLV-1-associated myelopathy/tropical spastic paraparesis(HAM/TSP) and infective dermatitis associated with HTLV-1 (IDH). Few data are available on PVL in the different clinical types of adult T-cell leukemia/lymphoma (ATL), a malignancy associated with HTLV-1. PVL assessment may constitute a useful tool for classifying types of ATL. The objective of this study was to assess the PVL levels of patients with different clinical types of ATL. The study included 39 samples from patients with the following clinical subtypes of ATL: acute (n = 11), chronic (n = 11), smoldering (n = 10), lymphoma (n = 5) and primary cutaneous tumoral (n = 2). PVL was quantified using quantitative real-time PCR, taking the tax region of provirus into consideration and using β-globulin as the reference gene. PVL levels were highest in the chronic and acute subtypes, but there was no statistically significant difference between these two subtypes (p = 0.6936). In smoldering ATL, PVL levels were lower compared to the levels found in the acute (p = 0.0124) and chronic (p = 0.0067) subtypes. In the primary cutaneous tumoral and lymphoma subtypes, PVL levels were intermediate but there were no statistically significant differences between these and the other clinical subtypes. The present results suggest that PVL levels in ATL are related to the lymphocytosis observed in the acute and chronic subtypes, but appear to be unrelated to the aggressiveness of the disease.