ArticlePLoS pathogens2025
HTLV-1 p12 is cleaved to p8 by the signal peptidase complex and its inhibition impairs p8-dependent transmission.
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 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Signal peptidase complex mediates rotavirus VP7 processing and virion assembly.PLoS pathogens · 2026Article
- Signal peptidase complex mediates rotavirus VP7 processing and virion assembly.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Infection with the oncogenic delta-retrovirus Human T-cell Leukemia Virus Type 1 (HTLV-1) causes aggressive CD4 + T-cell malignancy or progressive neuroinflammatory disorders after a long latency period. The HTLV-1 accessory protein p8 is cleaved from its precursor p12, and both proteins are required for viral persistence. Moreover, p8 enhances viral infectivity by inducing cell-cell contacts and cellular conduit formation. To date, host factors cleaving p12 to p8 remain unknown. Here, we report that p12 carries a signal peptide that is cleaved by the signal peptidase complex (SPC) to generate p8, and blocking of p12 cleavage correlated with a decreased cell aggregation and conduit formation, leading to impaired viral transmission of chronically HTLV-1 infected MT-2 cells. Bioinformatics identified p12 to carry a signal peptide, which is cleaved to generate p8. Inhibition of the SPC function by the SPC-specific inhibitor Cavinafungin and transient knockdown of SPC subunits confirmed the importance of the SPC to cleave p12 to p8. Mutational studies of the signal peptide sequence based on bioinformatics predictions generated cleavage-deficient p12 mutants and verified critical residues for signal peptide cleavage. Further, co-culture assays between Cavinafungin pre-treated chronically infected MT-2 cells, which transmit HTLV-1 dependent on p8, and Jurkat T-cells revealed a significantly impaired viral cell-cell transmission, suggesting that blockage of p12 cleavage interferes with p8-dependent HTLV-1 transmission. Imaging analysis confirmed that SPC-inhibition impairs cell aggregation in MT-2 cells and blocks p8-induced conduit formation in transfected Jurkat T-cells. Collectively, we identified the SPC as the host cell factor cleaving p12 to p8. Inhibition of p12 cleavage led to the absence of p8, which led to impaired cell-to-cell transmission, and coincided with the absence of p8-induced cell aggregation and conduit formation.
Indexed as
Identifiers
What OpenQuestion holds
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.