Evidence map›Paper›PMID 41758870›Full record

ArticlePLoS pathogens2026

PRRSV-2 impedes lysosomes from eliminating secondary infected bacteria.

Zifang Zheng, Xue Ling, Shuang Qiao, Jie Wu, Shuangquan Zhang, Xiao Liu, Yang Li, Caiyun Xie, Zhiqian Ma, Xuyang Guo and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS pathogens, 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. PRRSV suppresses ER-phagy through Nsp2- and Nsp5-mediated degradation of FAM134B.Frontiers in cellular and infection microbiology · 2026
    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

16 authors.

Zifang ZhengState 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.
Xue LingState 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.
Shuang QiaoState 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.
Jie WuState 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.
Shuangquan ZhangState 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.
Xiao 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.
Yang LiState 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.
Caiyun XieState 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.
Zhiqian MaState 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.
Xuyang GuoState 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.
Zhiwei LiState 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.
Yingtong FengState 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.
Lele XuState 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.
Jianwu ZhangState 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.
Haixue ZhengState 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.
Shuqi XiaoState 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 https://orcid.org/0000-0002-6468-2608

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As an immunosuppressive virus, the occurrence of secondary bacterial infection following porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2) infection is widely recognized. The immune escape capability of PRRSV-2 enables the virus to maintain efficient proliferation even within macrophages. In this study, we report that PRRSV-2 infection disrupts the intracellular F-actin, thereby causing the inability of macrophage lysosomes to transport to secondary infected bacteria promptly for bacterial clearance. RhoA is a crucial molecule in the polymerization of G-actin to F-actin within the cell. Silencing RhoA suppresses the production of F-actin in the cell, delays the targeted clearance of bacteria by lysosomes, and leads to an increase in the number of viable bacteria within the cell. Overexpression of RhoA promotes the production of F-actin, accelerates the targeted clearance of lysosomes to bacteria, and effectively reduces the number of viable bacteria. After PRRSV-2 infection, the expression of RhoA protein is down-regulated by nsp5 to inhibit the production of F-actin. Mechanistically, nsp5 interacts with the E3 ubiquitin ligase Smurf1 to mediate K63-linked ubiquitination of RhoA at lysine 187 (K187), which subsequently leads to its degradation via the autophagy-lysosome pathway under the guidance of the selective autophagy receptor TOLLIP. Therefore, our study presents a novel mechanism through which PRRSV-2 reprograms the cytoskeleton to facilitate the survival of bacteria in secondary infections, providing a theoretical foundation and target for the prevention and control of PRRSV-2 secondary bacterial infection.

Indexed as

Bacterial InfectionsCoinfectionLysosomesMacrophagesPorcine Reproductive and Respiratory SyndromePorcine respiratory and reproductive syndrome virusActinsAnimalsAutophagyrhoA GTP-Binding ProteinSwineActinsrhoA GTP-Binding Protein

Identifiers

PMID41758870
PMCPMC12959842

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Registered trials

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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.