ArticleJournal of virology2010
The clinically approved proteasome inhibitor PS-341 efficiently blocks influenza A virus and vesicular stomatitis virus propagation by establishing an antiviral state.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Bortezomib exhibited bacteriostatic activity and pro-inflammatory effect against Mycoplasma pneumoniae.The Journal of antibiotics · 2026Article
- CRISPR antiviral inhibits neurotrophic JC polyomavirus in 2D and 3D culture models through dual-gRNA excision by SaCas9.Molecular therapy. Nucleic acids · 2025Article
- A Review and Meta-Analysis of Influenza Interactome Studies.Frontiers in microbiology · 2022Review
- Review
- Proteomic Signature of Host Response to SARS-CoV-2 Infection in the Nasopharynx.Molecular & cellular proteomics : MCP · 2021Article
- Semisynthetic Cardenolides Acting as Antiviral Inhibitors of Influenza A Virus Replication by Preventing Polymerase Complex Formation.Molecules (Basel, Switzerland) · 2020Article
- The analgesic and anti-inflammatory effects of zukamu granules, a traditional Chinese medical formulation.Pharmaceutical biology · 2019Article
- Proteasome Inhibitor PS-341 Effectively Blocks Infection by the Severe Fever with Thrombocytopenia Syndrome Virus.Virologica Sinica · 2019Article
- Article
- Repurposing host-based therapeutics to control coronavirus and influenza virus.Drug discovery today · 2019Review
- A big data pipeline: Identifying dynamic gene regulatory networks from time-course Gene Expression Omnibus data with applications to influenza infection.Statistical methods in medical research · 2018Article
- The emerging influenza virus threat: status and new prospects for its therapy and control.Archives of virology · 2018Review
- A Mass Spectrometry-Based Profiling of Interactomes of Viral DDB1- and Cullin Ubiquitin Ligase-Binding Proteins Reveals NF-κB Inhibitory Activity of the HIV-2-Encoded Vpx.Frontiers in immunology · 2018Article
- Review
- Phosphorylation of influenza A virus NS1 protein at threonine 49 suppresses its interferon antagonistic activity.Cellular microbiology · 2016Article
- Broad-spectrum antiviral agents.Frontiers in microbiology · 2015Review
- The Modified JiuWei QiangHuo Decoction Alleviated Severe Lung Injury Induced by H1N1 Influenza Virus by Regulating the NF- κ B Pathway in Mice.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Bortezomib-induced unfolded protein response increases oncolytic HSV-1 replication resulting in synergistic antitumor effects.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Oncolytic vesicular stomatitis virus and bortezomib are antagonistic against myeloma cells in vitro but have additive anti-myeloma activity in vivo.Experimental hematology · 2013Article
- Obatoclax, saliphenylhalamide, and gemcitabine inhibit influenza a virus infection.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently it has been shown that the proinflammatory NF-kappaB pathway promotes efficient influenza virus propagation. Based on these findings, it was suggested that NF-kappaB blockade may be a promising approach for antiviral intervention. The classical virus-induced activation of the NF-kappaB pathway requires proteasomal degradation of the inhibitor of NF-kappaB, IkappaB. Therefore, we hypothesized that inhibition of proteasomal IkappaB degradation should impair influenza A virus (IAV) replication. We chose the specific proteasome inhibitor PS-341, which is a clinically approved anticancer drug also known as Bortezomib or Velcade. As expected, PS-341 treatment of infected A549 cells in a concentration range that was not toxic resulted in a significant reduction of progeny virus titers. However, we could not observe the proposed suppression of NF-kappaB-signaling in vitro. Rather, PS-341 treatment resulted in an induction of IkappaB degradation and activation of NF-kappaB as well as the JNK/AP-1 pathway. This coincides with enhanced expression of antiviral genes, such as interleukin-6 and, most importantly, MxA, which is a strong interferon (IFN)-induced suppressor of influenza virus replication. This suggests that PS-341 may act as an antiviral agent via induction of the type I IFN response. Accordingly, PS-341 did not affect virus titers in Vero cells, which lack type I IFN genes, but strongly inhibited replication of vesicular stomatitis virus (VSV), a highly IFN-sensitive pathogen. Thus, we conclude that PS-341 blocks IAV and VSV replication by inducing an antiviral state mediated by the NF-kappaB-dependent expression of antivirus-acting gene products.
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