ArticleFrontiers in microbiology2019
HTLV-1 Extracellular Vesicles Promote Cell-to-Cell Contact.
Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- Persistent Human T-Lymphotropic Virus Type 1 (HTLV-1) Infection in the Placenta of Pregnant Women.Journal of medical virology · 2025Article
- Inhibitors of Tax1-PDZ Interactions Block HTLV-1 Viral Transmission by Changing EV Composition.Journal of extracellular vesicles · 2025Article
- Extracellular vesicles as missiles for enhanced anti-tumor efficacy of oncolytic viruses: from disseminating oncolysis and anti-tumor immunity to targeted delivery.Cell communication and signaling : CCS · 2025Review
- A State-of-the-Art Review on the Recent Advances in Exosomes in Oncogenic Virus.Health science reports · 2024Article
- Current State of Therapeutics for HTLV-1.Viruses · 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
- Dissemination of the Flavivirus Subgenomic Replicon Genome and Viral Proteins by Extracellular Vesicles.Viruses · 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
- Review
- The transcriptome of HTLV-1-infected primary cells following reactivation reveals changes to host gene expression central to the proviral life cycle.PLoS pathogens · 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
- Mechanisms of Innate Immune Sensing of HTLV-1 and Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2023Review
- Extracellular Vesicles and Viruses: Two Intertwined Entities.International journal of molecular sciences · 2023Review
- Viral Immune signatures from cerebrospinal fluid extracellular vesicles and particles in HAM and other chronic neurological diseases.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Human T-cell leukemia virus-1 (HTLV-1) is a neglected and incurable retrovirus estimated to infect 5 to 10 million worldwide. Specific indigenous Australian populations report infection rates of more than 40%, suggesting a potential evolution of the virus with global implications. HTLV-1 causes adult T-cell leukemia/lymphoma (ATLL), and a neurological disease named HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). Even though HTLV-1 transmission primarily occurs from cell-to-cell, there is still a gap of knowledge regarding the mechanisms of viral spread and disease progression. We have recently shown that Extracellular Vesicles (EVs) ubiquitously produced by cells may be used by HTLV-1 to transport viral proteins and RNA, and elicit adverse effects on recipient uninfected cells. The viral proteins Tax and HBZ are involved in disease progression and impairment of autophagy in infected cells. Here, we show that activation of HTLV-1 via ionizing radiation (IR) causes a significant increase of intracellular Tax, but not EV-associated Tax. Also, lower density EVs from HTLV-1-infected cells, separated by an Iodixanol density gradient, are positive for gp61+++/Tax+++/HBZ+ proteins (HTLV-1 EVs). We found that HTLV-1 EVs are not infectious when tested in multiple cell lines. However, these EVs promote cell-to-cell contact of uninfected cells, a phenotype which was enhanced with IR, potentially promoting viral spread. We treated humanized NOG mice with HTLV-1 EVs prior to infection and observed an increase in viral RNA synthesis in mice compared to control (EVs from uninfected cells). Proviral DNA levels were also quantified in blood, lung, spleen, liver, and brain post-treatment with HTLV-1 EVs, and we observed a consistent increase in viral DNA levels across all tissues, especially the brain. Finally, we show direct implications of EVs in viral spread and disease progression and suggest a two-step model of infection including the release of EVs from donor cells and recruitment of recipient cells as well as an increase in recipient cell-to-cell contact promoting 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 OpenQuestion graph.