ArticlePLoS pathogens2025
Splicing-dependent restriction of the HBZ gene by Tax underlies biphasic HTLV-1 infection.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Viral persistence and host-state remodeling in virus-associated cancers.Archives of microbiology · 2026Review
- The mJournal of virology · 2026Article
- Preparation of soluble and functional recombinant HTLV-1 Tax protein using bacterial chaperones.Biology open · 2026Article
- PFV Tas protein recruits hnRNPF to promote the splicing of tas/bet pre-mRNA.Cell & bioscience · 2026Article
- Article
- Recent advances in infections as risk factors for lymphoma: a review of the effects of viral, bacterial, and fungal infections in lymphoma.Archives of microbiology · 2025Review
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Authors and funding
13 authors.
Funding
Abstract
HTLV-1 is an oncovirus that encodes a transactivator Tax and a regulatory gene HBZ. HTLV-1 early or infectious replication depends on Tax; during HTLV-1 late infection, HBZ plays a crucial role in driving the proliferation of infected cells and maintaining viral persistence. The biphasic replication pattern of HTLV-1 dictated by Tax and HBZ represents a result of viral host adaptation, but how HTLV-1 coordinates Tax and HBZ expression to facilitate early and late infection remains elusive. Here we reveal that HBZ RNA splicing exhibits distinct patterns in Tax+ and Tax- HTLV-1 infected cells. We demonstrate that Tax interacts with the host spliceosome and inhibits HBZ splicing by competitively binding splicing factors including WDR83 and GPATCH1. As a result, Tax confers a natural constraint on HBZ, counterbalancing its anti-replication effect at HTLV-1 early infection, while unleashing HBZ to drive HTLV-1 mitotic propagation during late infection. The splicing-dependent restriction of HBZ by Tax thus represents a critical interplay central to HTLV-1 persistence.
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Registered trials
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