Evidence map›Paper›PMID 42059595›Full record

ArticlemBio2026

Cross-utilization of viral polymerase: parainfluenza virus hijacks the RdRp of porcine sapelovirus to facilitate its replication during co-infection.

Jianing Chen, Shengyu Lin, Jiao Tang, Mengling Gao, Qianzi Liu, Jiawei Du, Chen Tan, Zhenli Gong, Libin Liang, Ting Zhu and 1 more

Abstract read
In one paragraph

Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Jianing Chen *State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.ORCID 0000-0002-9431-710X
Shengyu Lin *State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Jiao Tang *State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Mengling GaoState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Qianzi LiuState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Jiawei DuState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Chen TanState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Zhenli GongState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Libin LiangCollege of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, Shanxi, China.
Ting ZhuCollege of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, Fujian, China.
Guangliang LiuState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.ORCID 0000-0001-8158-5749

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parainfluenza virus is a significant respiratory pathogen affecting both humans and animals, capable of causing acute respiratory tract infections in infants and immunocompromised individuals. Recently, parainfluenza virus 5 (PIV5) has been frequently detected in swine diarrheal samples. However, experimental infections revealed that PIV5 alone induces only mild clinical symptoms. Further analysis suggested that co-infection with porcine sapelovirus (PSV) may underlie the observed disease severity. This hypothesis was confirmed through animal studies. Co-infection was shown to occur intracellularly, where PSV significantly enhanced PIV5 replication. Mechanistically, this effect was primarily mediated by PSV 3D, an RNA-dependent RNA polymerase (RdRp). PSV 3D directly interacted with PIV5 nucleoprotein and genomic RNA. Mini-genome assays demonstrated that PSV 3D substantially increased PIV5 genomic activity. Using an infectious cDNA clone of PIV5 and a series of mutants, we further confirmed that PSV 3D promoted transcription of both plus- and minus-strand PIV5 RNAs. Notably, RdRp (3D) proteins from two other picornaviruses also enhanced PIV5 RNA synthesis, suggesting a conserved function across picornaviruses. In summary, this study provides the first evidence that PIV5 hijacks the RdRp of a co-infecting virus from a different viral family to support its own replication. These findings advance our understanding of virus-virus interactions and offer a novel perspective in virology. IMPORTANCE: The gastrointestinal tract harbors a vast and diverse community of microorganisms, making it an ideal environment for exploring microbial interactions. While virus-bacteria interactions have been widely studied, virus-virus interactions remain largely uncharacterized. In this study, we demonstrated that porcine sapelovirus (PSV) and parainfluenza virus 5 (PIV5) co-infect cells and directly interact within the host. Specifically, the RNA-dependent RNA polymerase protein (3D) of PSV significantly promoted PIV5 replication by interacting with key components of the PIV5 ribonucleoprotein complex and enhancing the synthesis of both plus- and minus-strand viral RNAs. Similar effects were observed with the 3D proteins from two additional picornaviruses, suggesting a shared mechanism among picornaviruses in facilitating co-infecting virus replication. This work uncovers a novel cross-family polymerase hijacking event and provides important insights into virus-virus interactions, highlighting new potential targets for the control and prevention of swine enteric diseases.

Indexed as

CoinfectionParainfluenza Virus 5RNA-Dependent RNA PolymeraseViral ProteinsVirus ReplicationAnimalsCell LineHumansRNA ReplicationRNA, ViralSwineSwine DiseasesRNA-Dependent RNA PolymeraseRNA, ViralViral Proteinsco-infectionparainfluenza virus 5porcine sapelovirusRdRpvirus–virus interaction

Identifiers

PMID42059595
PMCPMC13251386

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.