ArticlePLoS pathogens2014
Regulation of human T-lymphotropic virus type I latency and reactivation by HBZ and Rex.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 57 citations in OpenAlex.
- A State-of-the-Art Review on the Recent Advances in Exosomes in Oncogenic Virus.Health science reports · 2024Article
- 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
- Adult T-Cell Lymphoma (ATL) With Erythroderma in Indolent Human T-Lymphotropic Virus Type I (HTLV-1) Infection.Cureus · 2023Article
- Origin and functional role of antisense transcription in endogenous and exogenous retroviruses.Retrovirology · 2023Review
- NF-κB-Induced R-Loops and Genomic Instability in HTLV-1-Infected and Adult T-Cell Leukemia Cells.Viruses · 2022Review
- Emerging roles for endogenous retroviruses in immune epigenetic regulation.Immunological reviews · 2022Review
- A newly identified interaction between nucleolar NPM1/B23 and the HTLV-I basic leucine zipper factor in HTLV-1 infected cells.Frontiers in microbiology · 2022Article
- Tuning Rex rules HTLV-1 pathogenesis.Frontiers in immunology · 2022Review
- NF-κB-induced R-loop accumulation and DNA damage select for nucleotide excision repair deficiencies in adult T cell leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- In vivo dynamics and adaptation of HTLV-1-infected clones under different clinical conditions.PLoS pathogens · 2021Article
- The versatile role of exosomes in human retroviral infections: from immunopathogenesis to clinical application.Cell & bioscience · 2021Review
- Human T-lymphotropic virus type 1 (HTLV-1) and cellular immune response in HTLV-1-associated myelopathy/tropical spastic paraparesis.Journal of neurovirology · 2020Review
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020Review
- RNF8 Dysregulation and Down-regulation During HTLV-1 Infection Promote Genomic Instability in Adult T-Cell Leukemia.PLoS pathogens · 2020Article
- The Complex Relationship between HTLV-1 and Nonsense-Mediated mRNA Decay (NMD).Pathogens (Basel, Switzerland) · 2020Review
- HTLV-1 bZIP factor: the key viral gene for pathogenesis.Retrovirology · 2020Review
- Cyclin-dependent kinases and CDK inhibitors in virus-associated cancers.Infectious agents and cancer · 2020Review
- HTLV-1 infection: An emerging risk. Pathogenesis, epidemiology, diagnosis and associated diseases.Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia · 2019Review
- Human T cell leukemia virus type 1 and Zika virus: tale of two reemerging viruses with neuropathological sequelae of public health concern.Journal of neurovirology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Human T lymphotropic virus type I (HTLV-I) infection is largely latent in infected persons. How HTLV-1 establishes latency and reactivates is unclear. Here we show that most HTLV-1-infected HeLa cells become senescent. By contrast, when NF-κB activity is blocked, senescence is averted, and infected cells continue to divide and chronically produce viral proteins. A small population of infected NF-κB-normal HeLa cells expresses low but detectable levels of Tax and Rex, albeit not Gag or Env. In these "latently" infected cells, HTLV-1 LTR trans-activation by Tax persists, but NF-κB trans-activation is attenuated due to inhibition by HBZ, the HTLV-1 antisense protein. Furthermore, Gag-Pol mRNA localizes primarily in the nuclei of these cells. Importantly, HBZ was found to inhibit Rex-mediated export of intron-containing mRNAs. Over-expression of Rex or shRNA-mediated silencing of HBZ led to viral reactivation. Importantly, strong NF-κB inhibition also reactivates HTLV-1. Hence, during HTLV-1 infection, when Tax/Rex expression is robust and dominant over HBZ, productive infection ensues with expression of structural proteins and NF-κB hyper-activation, which induces senescence. When Tax/Rex expression is muted and HBZ is dominant, latent infection is established with expression of regulatory (Tax/Rex/HBZ) but not structural proteins. HBZ maintains viral latency by down-regulating Tax-induced NF-κB activation and senescence, and by inhibiting Rex-mediated expression of viral structural proteins.
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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.