ArticlemBio2025
PRRSV promotes bacterial infection by remodeling actin cytoskeleton and cell membrane proteins.
Article in mBio, 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
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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
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Who cites it
2 citing papers in PubMed.
- Lectin-Based Antiviral Strategies for Porcine Reproductive and Respiratory Syndrome Virus 2 Infection: Griffithsin Suppresses Viral Replication In Vitro and Reduces Early Viremia In Vivo.Microorganisms · 2026Article
- Paradigm shift: PRRSV-mediated active remodeling of the host immune system-From epigenetic domestication to functional hijacking.Frontiers in microbiology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Secondary infection is a worldwide problem in the prevention and control of viral infection. Secondary bacterial infection induced by porcine reproductive and respiratory syndrome virus (PRRSV) infection causes enormous economic losses, but the relevant mechanism remains unclear. We found that the infection of IMPORTANCE: An important reason why porcine reproductive and respiratory syndrome virus (PRRSV) is difficult to control effectively is that it often causes severe secondary bacterial infections, which are usually attributed to the immunosuppression caused by PRRSV. However, the mechanism by which PRRSV infection leads to increased susceptibility of cells to bacterial infection has been largely overlooked. We revealed that PRRSV induced actin cytoskeleton rearrangement by upregulating FLNA expression, thereby aggravating bacterial invasion. PRRSV increased bacterial adhesion by promoting the ITGα5 expression, and the upregulation of ITGα5 could induce FLNA-mediated actin cytoskeleton rearrangement. Furthermore, we found that H1N1 and porcine circovirus type 2 infection also significantly promoted the expression of FLNA and ITGα5 and increased the infection of multiple bacteria. These results suggest that FLNA and ITGα5 play important roles in virus-induced secondary bacterial infection.
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