ArticleVirology2005
Porcine arterivirus activates the NF-kappaB pathway through IkappaB degradation.
Article in Virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 114 citations in OpenAlex.
- Advances in the immunosuppression of porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2026Review
- Proanthocyanidins carbon dots inhibit PRRSV infection by activating Nrf2/ARE to regulate oxidative stress and NLRP3 inflammasome-mediated pyroptosis.Veterinary research · 2025Article
- Article
- The mRNA and protein of IL-8 oppositely regulate PRRSV replication via nucleoprotein and 14-3-3γ.Journal of virology · 2025Article
- Porcine reproductive and respiratory syndrome virus nsp5 inhibits the activation of the Nrf2/HO-1 pathway by targeting p62 to antagonize its antiviral activity.Journal of virology · 2025Article
- Hesperetin Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication by Downregulating the P38/JUN/FOS Pathway In Vitro.Microorganisms · 2025Article
- Porcine reproductive and respiratory syndrome developments: An in-depth review of recent findings.Open veterinary journal · 2024Review
- Article
- Regulatory Non-Coding RNAs during Porcine Viral Infections: Potential Targets for Antiviral Therapy.Viruses · 2024Review
- Research progress on the N protein of porcine reproductive and respiratory syndrome virus.Frontiers in microbiology · 2024Review
- A Novel Polysaccharide fromAntioxidants (Basel, Switzerland) · 2023Article
- N-Acetyltransferase 9 Inhibits Porcine Reproductive and Respiratory Syndrome Virus Proliferation by N-Terminal Acetylation of the Structural Protein GP5.Microbiology spectrum · 2023Article
- Therapeutic efficacy of tylvalosin combined withFrontiers in veterinary science · 2023Article
- Construction of an infectious cloning system of porcine reproductive and respiratory syndrome virus and identification of glycoprotein 5 as a potential determinant of virulence and pathogenicity.Frontiers in microbiology · 2023Article
- Highly Pathogenic PRRSV-Infected Alveolar Macrophages Impair the Function of Pulmonary Microvascular Endothelial Cells.Viruses · 2022Article
- Andrographolide and Its Derivative Potassium Dehydrographolide Succinate Suppress PRRSV Replication in Primary and Established Cells via Differential Mechanisms of Action.Virologica Sinica · 2021Article
- Damage to intestinal barrier integrity in piglets caused by porcine reproductive and respiratory syndrome virus infection.Veterinary research · 2021Article
- Porcine Reproductive and Respiratory Syndrome Virus Evades Antiviral Innate ImmunityFrontiers in microbiology · 2021Review
- CD163 Antibodies Inhibit PRRSV Infection via Receptor Blocking and Transcription Suppression.Vaccines · 2020Article
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor-kappaB (NF-kappaB) is a critical regulator of innate and adaptive immune function as well as cell proliferation and survival. The present study demonstrated for the first time that a virus belonging to the Arteriviridae family activates NF-kappaB in MARC-145 cells and alveolar macrophages. In porcine reproductive and respiratory syndrome virus (PRRSV)-infected cells, NF-kappaB activation was characterized by translocation of NF-kappaB from the cytoplasm to the nucleus, increased DNA binding activity, and NF-kappaB-regulated gene expression. NF-kappaB activation was increased as PRRSV infection progressed and in a viral dose-dependent manner. UV-inactivation of PRRSV significantly reduced the level of NF-kappaB activation. Degradation of IkappaB protein was detected late in PRRSV infection, and overexpression of the dominant negative form of IkappaBalpha (IkappaBalphaDN) significantly suppressed NF-kappaB activation induced by PRRSV. However, IkappaBalphaDN did not affect viral replication and viral cytopathic effect. PRRSV infection induced oxidative stress in cells by generating reactive oxygen species (ROS), and antioxidants inhibited NF-kappaB DNA binding activity in PRRSV-infected cells, suggesting ROS as a mechanism by which NF-kappaB was activated by PRRSV infection. Moreover, NF-kappaB-dependent expression of matrix metalloproteinase (MMP)-2 and MMP-9 was observed in PRRSV-infected cells, an observation which implies that NF-kappaB activation is a biologically significant aspect of PRRSV pathogenesis. The results presented here provide a basis for understanding molecular pathways of pathology and immune evasion associated with disease caused by PRRSV.
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Registered trials
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.