Abstract
Human T lymphotropic virus type 1 (HTLV-1) is the etiological agent of HTLV-1-associated myelopathy, and adult T cell lymphoma/leukemia (ATL/L). Pulmonary complications such as alveolitis and bronchiectasis were found in individuals who develop TSP/HAM due to chronic inflammation. These individuals showed image anomalies in CT scans and changes in pulmonary function parameters distinctive of pulmonary disease. Furthermore, infected individuals have a greater susceptibility to pulmonary tuberculosis either due to changes in the innate immune response, in asymptomatic carriers, or to an opportunistic disease linked to immunodepression, in individuals who develop ATL/L. This summary addresses the general lack of knowledge regarding the relationship between HTLV-1 and pulmonary diseases and provides direction for future work.
Highlights
Human lymphotropic virus type 1 (HTLV-1) is the etiological agent of Human T lymphotropic virus type 1 (HTLV-1)-associated myelopathy, and adult T-cell lymphoma/leukemia (ATL/L) (Richardson et al, 1990)
Patients with HTLV-1 with pulmonary involvement exhibit an elevation of T lymphocytes in bronchoalveolar lavage fluid (BALF) and consequent pulmonary inflammation, which is mediated by a Th1 type immune response, characterized by the presence of soluble IL-2 receptors (IL-2R), increased levels of interleukins IL-2, IL-12, and interferon (IFN-γ) (Sugimoto et al, 1989; Yamazato et al, 2003; Nakayama et al, 2013)
There is an association between HTLV-1 infection and bronchiectasis (Honarbakhsh and Taylor, 2015)
Summary
Human T lymphotropic virus type 1 (HTLV-1) is the etiological agent of HTLV1-associated myelopathy, and adult T cell lymphoma/leukemia (ATL/L) Pulmonary complications such as alveolitis and bronchiectasis were found in individuals who develop TSP/HAM due to chronic inflammation. Infected individuals have a greater susceptibility to pulmonary tuberculosis either due to changes in the innate immune response, in asymptomatic carriers, or to an opportunistic disease linked to immunodepression, in individuals who develop ATL/L. This summary addresses the general lack of knowledge regarding the relationship between HTLV-1 and pulmonary diseases and provides direction for future work
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