ArticlemBio2024
PRRSV GP5 inhibits the antivirus effects of chaperone-mediated autophagy by targeting LAMP2A.
Article in mBio, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Review
- The S32 amino acid deletion in the GP5 protein modulates the infectivity of porcine reproductive and respiratory syndrome virus.Virulence · 2026Article
- Chaperone-mediated autophagy in physiological homeostasis, disease and ageing.Nature reviews. Molecular cell biology · 2026Review
- Article
- Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)-Induced Reactive Oxygen Species Inhibit Phagocytosis in Alveolar Macrophages.International journal of molecular sciences · 2026Article
- First Molecular Detection and Genetic Characterization of Porcine Circovirus 5 in Diagnostic Swine Samples from China.Veterinary sciences · 2026Article
- Senecavirus a VP2 protein orchestrates PRDX1 degradation through dual autophagy pathways: macroautophagy and chaperone-mediated autophagy.Autophagy · 2026Article
- PLCG1 promotes sevoflurane-induced neuronal ferroptosis by enhancing K63-linked ubiquitination and proteasomal degradation of LAMP2A.Experimental brain research · 2026Article
- Critical Roles and Molecular Mechanisms of Chaperone-Mediated Autophagy in Infections.International journal of molecular sciences · 2026Review
- PRRSV GP2a blocks the RLR signaling pathway by targeting RIG-I.Journal of virology · 2025Article
- A Porcine Monoclonal Antibody Targeting a Conserved GP4 Epitope Protects against In Vivo Infection via the Induction of Broad-Spectrum PRRSV Neutralization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- S146 and M148 within the mature chain domain of PSMB4 are crucial for degrading PRRSV nsp1α.Cellular and molecular life sciences : CMLS · 2025Article
- High glucose-induced PLCG1 histone acetylation to promote ferroptosis by LAMP2A/HSPA8 in a diabetic nephropathy model.Frontiers in pharmacology · 2025Article
- Calcium-mediated mitochondrial fission and mitophagy drive glycolysis to facilitate arterivirus proliferation.PLoS pathogens · 2025Article
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Authors and funding
9 authors.
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Abstract
Autophagy is an important biological process in host defense against viral infection. However, many viruses have evolved various strategies to disrupt the host antiviral system. Porcine reproductive and respiratory syndrome virus (PRRSV) is a typical immunosuppressive virus with a large economic impact on the swine industry. At present, studies on the escape mechanism of PRRSV in the autophagy process, especially through chaperone-mediated autophagy (CMA), are limited. This study confirmed that PRRSV glycoprotein 5 (GP5) could disrupt the formation of the GFAP-LAMP2A complex by inhibiting the MTORC2/PHLPP1/GFAP pathway, promoting the dissociation of the pGFAP-EF1α complex, and blocking the K63-linked polyubiquitination of LAMP2A to inhibit the activity of CMA. Further research demonstrated that CMA plays an anti-PRRSV role by antagonizing nonstructural protein 11 (NSP11)-mediated inhibition of type I interferon (IFN-I) signaling. Taken together, these results indicate that PRRSV GP5 inhibits the antiviral effect of CMA by targeting LAMP2A. This research provides new insight into the escape mechanism of immunosuppressive viruses in CMA. IMPORTANCE: Viruses have evolved sophisticated mechanisms to manipulate autophagy to evade degradation and immune responses. Porcine reproductive and respiratory syndrome virus (PRRSV) is a typical immunosuppressive virus that causes enormous economic losses in the swine industry. However, the mechanism by which PRRSV manipulates autophagy to defend against host antiviral effects remains unclear. In this study, we found that PRRSV GP5 interacts with LAMP2A and disrupts the formation of the GFAP-LAMP2A complex, thus inhibiting the activity of CMA and subsequently enhancing the inhibitory effect of the NSP11-mediated IFN-I signaling pathway, ultimately facilitating PRRSV replication. Our study revealed a novel mechanism by which PRRSV escapes host antiviral effects through CMA, providing a potential host target, LAMP2A, for developing antiviral drugs and contributing to understanding the escape mechanism of immunosuppressive viruses.
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