Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0140-6736(90)92542-p | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
rs179008 (A/T) and rs3853839 (C/G) polymorphisms are associated with variations in IFN-α levels in HTLV-1 infection.
Front Immunol
December 2024
Laboratory of Virology, Institute of Biological Sciences, Federal University of Pará, Belém, Brazil.
Article Synopsis
- The study investigates how genetic variations in the TLR7 gene impact responses to HTLV-1 infection, focusing on cytokine production and disease symptoms.
- Researchers analyzed blood samples from HTLV-1 infected individuals, including those with inflammatory diseases and asymptomatic cases, alongside controls, using techniques like PCR and ELISA.
- Findings indicated that specific genetic variations (polymorphisms) affect levels of immune responses, with some variants linked to higher levels of antiviral activity, though they did not correlate with disease symptoms.
Evaluation of ALKBH2 and ALKBH3 gene regulation in patients with adult T-cell leukemia/lymphoma.
Virol J
December 2024
Department of Microbiology, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Background: Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic virus that causes malignant adult T-cell leukemia/lymphoma (ATL). Patients infected with HTLV-1 are considered HTLV-1 carriers, and a small proportion of patients progress to life-threatening ATL after a long asymptomatic phase. No antiviral agent or preventive vaccine specific for HTLV-1 infection is established in current situation.
View Article and Find Full Text PDFHTLV-1 infected T cells cause bone loss via small extracellular vesicles.
J Extracell Vesicles
October 2024
Division of Bone & Mineral Diseases, Musculoskeletal Research Center, Washington University School of Medicine, Saint Louis, Missouri, USA.
Adult T cell leukaemia (ATL), caused by infection with human T- lymphotropic virus type 1 (HTLV-1), is often complicated by hypercalcemia and osteolytic lesions. Therefore, we studied the communication between patient-derived ATL cells (ATL-PDX) and HTLV-1 immortalized CD4+ T cell lines (HTLV/T) with osteoclasts and their effects on bone mass in mice. Intratibial inoculation of some HTLV/T leads to a profound local decrease in bone mass similar to marrow-replacing ATL-PDX, despite the fact that few HTLV/T cells persisted in the bone.
View Article and Find Full Text PDFDendritic Cells Pulsed with HAM/TSP Exosomes Sensitize CD4 T Cells to Enhance HTLV-1 Infection, Induce Helper T-Cell Polarization, and Decrease Cytotoxic T-Cell Response.
Viruses
September 2024
Department of Microbiology & Immunology, Drexel University College of Medicine, Philadelphia, PA 19129, USA.
HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive demyelinating disease of the spinal cord due to chronic inflammation. Hallmarks of disease pathology include dysfunctional anti-viral responses and the infiltration of HTLV-1-infected CD4+ T cells and HTLV-1-specific CD8+ T cells in the central nervous system. HAM/TSP individuals exhibit CD4+ and CD8+ T cells with elevated co-expression of multiple inhibitory immune checkpoint proteins (ICPs), but ICP blockade strategies can only partially restore CD8+ T-cell effector function.
View Article and Find Full Text PDFA New Strategy for Adult T-Cell Leukemia Treatment Targeting Glycogen Synthase Kinase-3β.
Eur J Haematol
December 2024
Department of Microbiology and Oncology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Japan.
Objectives: The role of glycogen synthase kinase (GSK)-3β in adult T-cell leukemia (ATL) caused by human T-cell leukemia virus type 1 (HTLV-1) is paradoxical and enigmatic. Here, we investigated the role of GSK-3β and its potential as a therapeutic target for ATL.
Methods: Cell proliferation/survival, cell cycle, apoptosis, and reactive oxygen species (ROS) generation were examined using the WST-8 assay, flow cytometry, and Hoechst 33342 staining, respectively.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!