An Overview of Human T-Lymphotropic Virus Type 1 Lung Injury

Previous studies have demonstrated the development of pulmonary impairment in individuals infected with human T-lymphotropic virus type 1 (HTLV-1). Complications, such as alveolitis and bronchiectasis, were found in individuals who developed tropical spastic paraparesis/HTLV-1-associated myelopathy...

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Published in:Frontiers in immunology Vol. 13; p. 914498
Main Authors: Dias, Ápio Ricardo Nazareth, Falcão, Luiz Fábio Magno, Quaresma, Juarez Antônio Simões
Format: Journal Article
Language:English
Published: Frontiers Media S.A 01-07-2022
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Summary:Previous studies have demonstrated the development of pulmonary impairment in individuals infected with human T-lymphotropic virus type 1 (HTLV-1). Complications, such as alveolitis and bronchiectasis, were found in individuals who developed tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP-HAM) due to chronic inflammation. These patients exhibited increased levels of lymphocytes (CD4+ and CD25+), cytokines (IL-2, IL-12, and IFN-γ), inflammatory chemokines (MIP-1α and IP-10), and cell adhesion molecules (ICAM-1) in the bronchoalveolar lavage fluid, with the result of chronic inflammation and lung injury. The main lesions observed at Chest high-resolution computed tomography were centrilobular nodules, parenchymal bands, lung cysts, bronchiectasis, ground-glass opacity, mosaic attenuation, and pleural thickening. It can lead to progressive changes in pulmonary function with the development of restrictive and obstructive diseases. Recent studies suggest a causal relationship between HTLV-1 and pulmonary diseases, with intensification of lesions and progressive decrease in pulmonary function. This summary updates a previous publication and addresses the general lack of knowledge regarding the relationship between TSP-HAM and pulmonary disease, providing direction for future work and the management of these individuals.
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Reviewed by: Yoshihisa Yamano, St. Marianna University School of Medicine, Japan
These authors have contributed equally to this work
This article was submitted to Viral Immunology, a section of the journal Frontiers in Immunology
Edited by: Steven Jacobson, National Institute of Neurological Disorders and Stroke (NIH), United States
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.914498