ArticleViruses2020
Porcine Reproductive and Respiratory Syndrome Virus Antagonizes PCSK9's Antiviral Effect via Nsp11 Endoribonuclease Activity.
Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- PRRSV Nsp11 antagonizes host antiviral immune response by reducing OAS1 and RNase L expressions.BMC veterinary research · 2026Article
- Advances in the immunosuppression of porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2026Review
- PCSK9 inhibitors: a promising lipid-lowering strategy for kidney transplant recipients.Renal failure · 2025Review
- Strategies and scheming: the war between PRRSV and host cells.Virology journal · 2025Review
- Innate Immune Evasion of PRRSV nsp11 through Degradation of the HDAC2 by Its Endoribonuclease Activity.Viruses · 2024Article
- BST2 negatively regulates porcine reproductive and respiratory syndrome virus replication by restricting the expression of viral proteins.Virus research · 2023Article
- Research Progress on NSP11 of Porcine Reproductive and Respiratory Syndrome Virus.Veterinary sciences · 2023Review
- Recent advances in inhibition of porcine reproductive and respiratory syndrome virus through targeting CD163.Frontiers in microbiology · 2022Review
- Evasion of Antiviral Innate Immunity by Porcine Reproductive and Respiratory Syndrome Virus.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most important pathogens in the swine industry worldwide. Our previous study had indicated that proprotein convertase subtilisin/kexin type 9 (PCSK9) was a responsive gene in porcine alveolar macrophages (PAMs) upon PRRSV infection. However, whether PCSK9 impacts the PRRSV replication and how the PRRSV modulates host PCSK9 remains elusive. Here, we demonstrated that PCSK9 protein suppressed the replication of both type-1 and type-2 PRRSV species. More specifically, the C-terminal domain of PCSK9 was responsible for the antiviral activity. Besides, we showed that PCSK9 inhibited PRRSV replication by targeting the virus receptor CD163 for degradation through the lysosome. In turn, PRRSV could down-regulate the expression of PCSK9 in both PAMs and MARC-145 cells. By screening the nonstructural proteins (nsps) of PRRSV, we showed that nsp11 could antagonize PCSK9's antiviral activity. Furthermore, mutagenic analyses of PRRSV nsp11 revealed that the endoribonuclease activity of nsp11 was critical for antagonizing the antiviral effect of PCSK9. Collectively, our data provide further insights into the interaction between PRRSV and the cell host and offer a new potential target for the antiviral therapy of PRRSV.
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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.