ArticleJournal of virology2025
Lnc-DARVR/miR-365-1-5p/LAMB1 axis regulates rotavirus replication via the complement C3 pathway.
Article in Journal of virology, 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.
- Article
- Animal virus-host interactions mediated by non-coding RNAs.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antiviral effectors and cytokines are critical components of host innate immunity. However, the regulatory mechanisms governing the roles of these molecules in host-virus interactions are still unclear. Although long non-coding RNAs (lncRNAs) have been recognized as key players in various biological processes, their involvement in the complement system of host antiviral defenses remains to be explored. In this study, we discovered a novel, unannotated lncRNA, called DARVR. DARVR was found to be an intergenic lncRNA and inhibited rotavirus (RV) replication in MA104 cells. Mechanistically, we found that complement 3 (C3) was upregulated following RV infection in a LAMB1-dependent manner. However, LAMB1 expression was downregulated by miR-365-1-5p, resulting in the inhibition of the C3-mediated antiviral reaction. However, DARVR functioned as a competing endogenous RNA against miR-365-1-5p, promoting the expression of LAMB1 and thereby enhancing C3 activity and inhibiting RV replication. These results not only provide evidence demonstrating the involvement of lncRNAs in the regulation of RV infection but also highlight the role of complement factors in host innate immunity. IMPORTANCE: Long non-coding RNAs (lncRNAs) play versatile and critical roles in host-virus interactions, offering significant potential for developing targeted therapies to prevent or treat viral infections. Despite their importance, the involvement of lncRNAs in rotavirus infection remains underexplored. This study identifies a novel lncRNA that enhances complement factor C3 activity through the competing endogenous RNA (ceRNA) mechanism, effectively inhibiting rotavirus replication across different subtypes. These findings underscore the complex molecular interplay regulating complement factor activity during rotavirus infection and provide valuable insights into the host's antiviral mechanisms. This research paves the way for innovative therapeutic strategies targeting lncRNAs and complement factors to combat viral infections more effectively.
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.