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Human T-lymphotropic virus-1 (HTLV-1) induces neoplastic adult T-cell leukemia/lymphoma (ATLL) and neurological HTLV-1 associated myelopathy (HAM) in approximately 3 %-5 % of infected individuals. The precise factors that facilitate disease manifestation are still unknown; interaction between the virus and the host's immune response is key. Cytokines regulates physiological activities and their dysregulation may initiate the pathogenesis of various malignant and infectious diseases. Genetic variations, particularly polymorphisms in gene regulatory regions, lead to varying cytokine production patterns. Interferon-gamma (IFN-γ), a key cytokine in HTLV-1 infection, is a signature cytokine for T-helper 1 (Th1) cells that interferes with viral replication and enhances innate and adaptive immune responses during viral infections. The IFNG gene possesses several single nucleotide polymorphisms (SNPs), among which the + 874 A/T SNP has been widely studied for its functional role in HTLV-1 infection. The purpose of this review was to provide insight into the impact of IFNG SNPs on HTLV-1 Infection.
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http://dx.doi.org/10.1016/j.critrevonc.2025.104614 | DOI Listing |
J Med Virol
September 2025
Laboratory of Dermatology and Immunodeficiencies, Department of Dermatology, University of São Paulo Medical School, São Paulo, Brazil.
Mother-to-child transmission (MTCT) is the primary route of human T-lymphotropic virus type 1 (HTLV-1) infection. Although formula feeding reduces breastfeeding-associated transmission, MTCT still occurs, implicating pregnancy or delivery as key transmission windows. In this study, placental tissues from nine HTLV-1-positive mothers were analyzed using DNA/RNAscope, revealing low HTLV-1 DNA and RNA levels and a low RNA/DNA ratio, consistent with latent infection in the placenta and potentially explaining the low MTCT rate.
View Article and Find Full Text PDFInt J Hematol
September 2025
Department of Hematology/Oncology, Research Hospital, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan.
Adult T-cell leukemia-lymphoma (ATL) is one of the most intractable peripheral T-cell neoplasms caused by human T-cell leukemia virus type I (HTLV-1) infection. Recently, the incidence of HTLV-1 infection and ATL has increased in non-endemic metropolitan areas in Japan. This retrospective study evaluated the clinical features and outcomes of patients with aggressive ATL aged 70 years or younger treated at a core hospital in Tokyo between 2004 and 2016.
View Article and Find Full Text PDFFront Cell Infect Microbiol
September 2025
One Health Research Group, Faculty of Health Science, Universidad de Las Americas, Quito, Ecuador.
The human T-cell lymphotropic virus type 1 (HTLV-1) is a highly oncogenic retrovirus recognized as the causative agent of adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Among the key risk factors for ATLL development are high proviral load, reduced anti-Tax immune responses, and elevated levels of soluble interleukin-2 receptor. Unlike classical oncogenic viruses, HTLV-1 does not encode proto-oncogenes but instead drives cellular transformation through a combination of mechanisms, including viral gene dysregulation, chromatin remodeling, epigenetic reprogramming, persistent clonal expansion, immune evasion, and RNA-based modifications.
View Article and Find Full Text PDFPLoS Negl Trop Dis
August 2025
Centro Integrativo e Multidisciplinar de HTLV, Centro de Neurociências Escola Bahiana de Medicina e Saúde Pública, Salvador, Brazil.
Background: Human T-cell leukemia virus type 1 (HTLV-1) causes inflammatory diseases and is associated with various muscle abnormalities, including polymyositis. Elevated serum creatine kinase (CPK) levels are typically indicative of muscle damage.
Aims: This study aimed to determine the prevalence of HTLV-1 associated inflammatory myopathies (HAIM) in a large cohort of People living with HTLV-1 from Salvador, Brazil.
Front Cell Infect Microbiol
August 2025
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará, Belém, Brazil.
Introduction: Alterations in the immune response may influence the development of HTLV-1-associated diseases. TLR3 detects viral nucleic acids, including HTLV-1, and triggers the production of IFN-I and other cytokines. Genetic variations in may alter the antiviral and inflammatory responses and contribute to the progression of HTLV-1 infection.
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