ArticleJournal of virology2025
Galectin 3-binding protein suppresses PRRSV replication via Cullin3-mediated ubiquitination degradation of non-structural protein 12.
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 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Pathogenicity and virulence of PRRSV: From regulated cell death reprogramming landscape and immune subversion to precision vaccinology.Virulence · 2026Review
- RNF187 inhibits porcine reproductive and respiratory syndrome virus replication by recruiting the autophagy receptor NDP52 to degrade nsp12.Veterinary research · 2026Article
- Adaptive mutations at lysine residues of PRRSV-2 nsp12 enable evasion of host proteasomal degradation to promote subgenomic RNA synthesis.Journal of virology · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) poses a major threat to the global swine industry, yet effective antiviral strategies remain limited. This study identifies galectin 3-binding protein (LGALS3BP) as a critical host factor inhibiting PRRSV infection through targeting the viral conserved non-structural protein 12 (nsp12), a key component of the viral replication-transcription complex. Overexpression of LGALS3BP significantly suppressed PRRSV replication, while its knockdown enhanced viral replication. Mechanistically, LGALS3BP recruits the Cullin3 E3 ubiquitin ligase via its BACK domain to mediate the ubiquitination of nsp12 at lysine residue 91, leading to proteasomal degradation. This process disrupts nsp12-dependent synthesis of viral subgenomic RNA, thereby disrupting replication. Additionally, LGALS3BP enhances antiviral innate immunity by upregulating interferon (IFN)-β and IFN-stimulated genes (ISGs). The antiviral effect of LGALS3BP is conserved across diverse PRRSV strains, highlighting its broad-spectrum potential. These findings reveal a dual mechanism whereby LGALS3BP restricts PRRSV through direct degradation of a critical viral enzyme and modulation of host immune responses, highlighting LGALS3BP as a promising therapeutic avenue for PRRSV control.IMPORTANCEPorcine reproductive and respiratory syndrome virus (PRRSV) remains a major challenge to global swine production due to its genetic diversity, rapid mutation rate, and ability to evade host immunity. The nsp12 is highly conserved across PRRSV strains and plays a crucial role in viral RNA synthesis. This study identifies LGALS3BP as a critical host factor that inhibits PRRSV infection by targeting nsp12 via the ubiquitin-proteasome pathway. By uncovering this novel antiviral mechanism, the research highlights LGALS3BP as a promising therapeutic target for PRRSV control. Moreover, it contributes to our understanding of how host factors modulate viral replication and immunity, opening new avenues for developing host-targeted antiviral strategies. These findings have the potential to mitigate PRRSV-driven economic losses and improve swine health worldwide.
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