ArticleRetrovirology2021
Extracellular vesicles from HTLV-1 infected cells modulate target cells and viral spread.
Article in Retrovirology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 39 citations in OpenAlex.
- HTLV-1-Derived Exosomes Drive Transcriptional Reprogramming of Monocytes Toward a Mixed M1/M2 Phenotype in HAM/TSP.Pathogens (Basel, Switzerland) · 2026Article
- Macrophages in oncoviral infections: from immune regulators to therapeutic targets.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Review
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- In Vitro Model of the Human Blood-Brain Barrier to Explore HTLV-1 Immunopathogenesis.Current issues in molecular biology · 2025Article
- HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States.Viruses · 2025Review
- A Novel Tax-Responsive Reporter T-Cell Line to Analyze Infection of HTLV-1.Pathogens (Basel, Switzerland) · 2024Article
- Organoids and organoid extracellular vesicles-based disease treatment strategies.Journal of nanobiotechnology · 2024Review
- HTLV-1 infected T cells cause bone loss via small extracellular vesicles.Journal of extracellular vesicles · 2024Article
- Peculiar transcriptional reprogramming with functional impairment of dendritic cells upon exposure to transformed HTLV-1-infected cells.PLoS pathogens · 2024Article
- Oncoviral Infections and Small Extracellular Vesicles.Viruses · 2024Review
- Extracellular vesicle isolation methods identify distinct HIV-1 particles released from chronically infected T-cells.Journal of extracellular vesicles · 2024Article
- Purification Method of Extracellular Vesicles Derived from Human T-Cell Leukemia Virus Type 1-Infected Cells without Virions.Viruses · 2024Article
- Intercellular Transport of Viral Proteins.Results and problems in cell differentiation · 2024Review
- Engineered small extracellular vesicles as a novel platform to suppress human oncovirus-associated cancers.Infectious agents and cancer · 2023Review
- Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets.International journal of molecular sciences · 2023Review
- The helicase-like transcription factor redirects the autophagic flux and restricts human T cell leukemia virus type 1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Retroviral b-Zip protein (HBZ) contributes to the release of soluble and exosomal immune checkpoint molecules in the context of neuroinflammation.Journal of extracellular biology · 2023Article
- How Can We Prevent Mother-to-Child Transmission of HTLV-1?International journal of molecular sciences · 2023Review
- Extracellular Vesicles and Viruses: Two Intertwined Entities.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe Human T-cell Lymphotropic Virus Type-1 (HTLV-1) is a blood-borne pathogen and etiological agent of Adult T-cell Leukemia/Lymphoma (ATLL) and HTLV-1 Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). HTLV-1 has currently infected up to 10 million globally with highly endemic areas in Japan, Africa, the Caribbean and South America. We have previously shown that Extracellular Vesicles (EVs) enhance HTLV-1 transmission by promoting cell-cell contact.
resultsHere, we separated EVs into subpopulations using differential ultracentrifugation (DUC) at speeds of 2 k (2000×g), 10 k (10,000×g), and 100 k (100,000×g) from infected cell supernatants. Proteomic analysis revealed that EVs contain the highest viral/host protein abundance in the 2 k subpopulation (2 k > 10 k > 100 k). The 2 k and 10 k populations contained viral proteins (i.e., p19 and Tax), and autophagy proteins (i.e., LC3 and p62) suggesting presence of autophagosomes as well as core histones. Interestingly, the use of 2 k EVs in an angiogenesis assay (mesenchymal stem cells + endothelial cells) caused deterioration of vascular-like-tubules. Cells commonly associated with the neurovascular unit (i.e., astrocytes, neurons, and macrophages) in the blood-brain barrier (BBB) showed that HTLV-1 EVs may induce expression of cytokines involved in migration (i.e., IL-8; 100 k > 2 k > 10 k) from astrocytes and monocyte-derived macrophages (i.e., IL-8; 2 k > 10 k). Finally, we found that EVs were able to promote cell-cell contact and viral transmission in monocytic cell-derived dendritic cell. The EVs from both 2 k and 10 k increased HTLV-1 spread in a humanized mouse model, as evidenced by an increase in proviral DNA and RNA in the Blood, Lymph Node, and Spleen.
conclusionsAltogether, these data suggest that various EV subpopulations induce cytokine expression, tissue damage, and viral spread.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.