ArticleViruses2026
African Swine Fever Virus DP71L Protein Inhibits Dextran Sulfate Sodium (DSS)-Induced Murine Colitis.
Article in Viruses, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functions of most proteins encoded by the African swine fever virus (ASFV) remain largely unknown, although several have been reported to possess immunomodulatory properties. Among these, we identified that the DP71L protein exerts an inhibitory effect on inflammatory bowel disease. To investigate its protective role in murine colitis, we constructed and expressed a recombinant DP71L protein. Colitis was induced in mice using DSS, and the effects of DP71L treatment were evaluated by assessing histopathological changes, inflammatory cytokine profiles, oxidative stress markers, colonic tissue pathology, and the expression of tight-junction proteins (claudin-1, occludin, and ZO-1). Our results showed that DP71L intervention significantly attenuated body weight loss and organ damage and ameliorated DSS-induced colonic histopathological injury. Moreover, DP71L treatment markedly increased superoxide dismutase (SOD) activity and reduced malondialdehyde (MDA) content in colonic tissues. Mechanistically, DP71L suppressed both DSS-induced NF-κB and JAK-STAT activation and concurrently inhibited DSS-induced epithelial cell apoptosis. These events likely underlie the observed reduction in pro-inflammatory cytokines (IL-1β, IL-6, IFN-γ, and TNF-α) and the restoration of tight-junction protein expression, as DP71L treatment effectively prevented DSS-induced downregulation of claudin-1, occludin, and ZO-1, while also promoting the anti-inflammatory cytokines IL-10 and TGF-β. Collectively, our findings demonstrate that DP71L effectively inhibits the progression of murine colitis through coordinated anti-inflammatory and anti-apoptotic mechanisms. This study suggests that DP71L may function as a potential immunosuppressant, opening new avenues for the application of viral proteins in the treatment of immune-related disorders.
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.