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HUMAN T LYMPHOTROPIC VIRUS TYPE 1 (HTLV-1) PROVIRAL LOAD INDUCES ACTIVATION OF T-LYMPHOCYTES IN ASYMPTOMATIC CARRIERS.
Author
Affilliation
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil / Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil
Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil / Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil / Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil / Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil
Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil / Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Laboratório Avançado de Saúde Pública. Salvador, BA, Brasil / Bahiana School of Medicine and Public Health. Salvador, BA, Brasil
Abstract
Background: High HTLV-1 proviral load (PVL) is mainly found in infected individuals with HTLV-1-associated
myelopathy/tropical spastic paraparesis (HAM/TSP). However one third of asymptomatic carriers may have high PVL.
This study aimed to evaluate the impact of PVL in the activation of T lymphocytes of asymptomatic individuals
infected with HTLV-1.
Methods: Membrane activation markers (CD25+, CD28+, CD45RO+, CD69+, CD62L+, HLA-DR+), FoxP3+ and intracellular
IFN-γ expression were evaluated on both CD4+ and CD8+ T-lymphocytes from asymptomatic carriers with PVL ≥
and < 1% of infected cells, using flow cytometry. HTLV-1 proviral load was determined using real-time PCR.
Results: Asymptomatic carriers with PVL ≥ 1% presented a higher frequency of CD4+CD25+CD45RO+ (13.2% vs. 4%,
p = 0.02), CD4+HLA-DR+ (18% vs. 8.3%, p = 0.01) and CD4+IFN-γ+ (4.5%; 1%, p = 0.01) T-cells, than healthy donors.
HTLV-1 PVL was directly correlated with the proportion of CD4+CD25+CD45RO+ T-cells (R = 0.7, p = 0.003). Moreover, a
significant increase in the proportion of CD4 + FoxP3+ T-cells was observed in HTLV-1-infected individuals, compared
to healthy donors.
Conclusion: HTLV-1 PVL is associated with activation of both CD4+ and CD8+ T-lymphocytes in asymptomatic
individuals. Prospective studies should be conducted to evaluate whether asymptomatic individuals with higher PVL
and high immune activation are more prone to developing HTLV-1-associated diseases
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