ArticleFrontiers in microbiology2021
Induction of UPR Promotes Interferon Response to Inhibit PRRSV Replication
Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- The host protein SSR4 mediates PRRSV-induced endoplasmic reticulum stress via interaction with Nsp2.Journal of virology · 2026Article
- In vivo quantitative proteomic analysis of porcine alveolar macrophages in PRRSV-infected pigs.Virologica Sinica · 2025Article
- A Live-Attenuated Chimeric Vaccine Candidate Against the Emerging NADC34-Like PRRSV.Veterinary sciences · 2025Article
- Enhanced Porcine Reproductive and Respiratory Syndrome Virus Replication in Nsp4- or Nsp2-Overexpressed Marc-145 Cell Lines.Veterinary sciences · 2025Article
- Swine NONO promotes IRF3-mediated antiviral immune response by Detecting PRRSV N protein.PLoS pathogens · 2024Article
- Viral Infections and Their Ability to Modulate Endoplasmic Reticulum Stress Response Pathways.Viruses · 2024Review
- Endoplasmic Reticulum Stress in Hypertension and Salt Sensitivity of Blood Pressure.Current hypertension reports · 2024Review
- Glycyrrhiza polysaccharides inhibits PRRSV replication.Virology journal · 2023Article
- The Antiviral Compound PSP Inhibits HIV-1 Entry via PKR-Dependent Activation in Monocytic Cells.Viruses · 2023Article
- LGP2 Promotes Type I Interferon Production To Inhibit PRRSV Infection via Enhancing MDA5-Mediated Signaling.Journal of virology · 2023Article
- Signaling Lymphocytic Activation Molecule Family Member 1 Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication.Animals : an open access journal from MDPI · 2022Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) was previously shown to induce a certain level of cellular stress during viral replication. Unfolded protein response (UPR) is a cellular stress response responsible for coping with stress and cellular survival. However, the pathway leading to the induction of UPR that may influence PRRSV replication is still unknown. Here, we found that PRRSV infection induced UPR prior to interferon response. Induction of UPR significantly enhanced the expression of interferon and interferon-related genes, thus leading to the suppression of PRRSV infection. Next, we explored the underlying mechanisms of UPR-induced antiviral response. We found that induction of UPR promoted the expression of protein kinase R (PKR), and PKR was highly correlated with the reduction of PRRSV replication. Furthermore, tunicamycin stimulation and PKR overexpression activated NF-κB and interferon response at the early stage of PRRSV infection, thus reinforcing the expression of type I interferons and proinflammatory cytokines and leading to inhibition of PRRSV. In addition, PRRSV nsp4 was shown to reduce the expression of PKR. These findings might have implications for our understandings of the host's immune mechanism against PRRSV and a new strategy of PRRSV to evade the host antiviral immunity.
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