ArticleViruses2016
Suppressive Effects of the Site 1 Protease (S1P) Inhibitor, PF-429242, on Dengue Virus Propagation.
Article in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Site-1 protease mediated GPC processing is required for persistence of LCMV Clone 13.Npj viruses · 2026Article
- Dengue virus and lipid metabolism: unravelling the interplay for future therapeutic approaches.Emerging microbes & infections · 2025Review
- Lipid Droplets: Formation, Degradation, and Their Role in Cellular Responses to Flavivirus Infections.Microorganisms · 2024Review
- Article
- The proprotein convertase SKI-1/S1P is a critical host factor for Nairobi sheep disease virus infectivity.Virus research · 2023Article
- Article
- Acetyl-CoA Carboxylase (ACC) Inhibitor, CP640186, Effectively Inhibited Dengue Virus (DENV) Infection via Regulating ACC Phosphorylation.Molecules (Basel, Switzerland) · 2022Article
- SREBP1 site 1 protease inhibitor PF-429242 suppresses renal cell carcinoma cell growth.Cell death & disease · 2021Article
- How Do Enveloped Viruses Exploit the Secretory Proprotein Convertases to Regulate Infectivity and Spread?Viruses · 2021Review
- PF-429242, a Subtilisin Inhibitor, Is EffectiveFrontiers in microbiology · 2021Article
- Dengue and Zika Viruses: Epidemiological History, Potential Therapies, and Promising Vaccines.Tropical medicine and infectious disease · 2020Review
- A mutation in Site-1 Protease is associated with a complex phenotype that includes episodic hyperCKemia and focal myoedema.Molecular genetics & genomic medicine · 2019Article
- Lipid Metabolism as a Source of Druggable Targets for Antiviral Discovery against Zika and Other Flaviviruses.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Hemorrhagic Fever-Causing Arenaviruses: Lethal Pathogens and Potent Immune Suppressors.Frontiers in immunology · 2019Review
- Antiviral Activity of Nordihydroguaiaretic Acid and Its Derivative Tetra-Antimicrobial agents and chemotherapy · 2017Article
- Modulation of Lipid Droplet Metabolism-A Potential Target for Therapeutic Intervention inFrontiers in microbiology · 2017Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dengue virus (DENV) infection causes one of the most widespread mosquito-borne diseases in the world. Despite the great need, effective vaccines and practical antiviral therapies are still under development. Intracellular lipid levels are regulated by sterol regulatory elements-binding proteins (SREBPs), which are activated by serine protease, site 1 protease (S1P). Small compound PF-429242 is known as a S1P inhibitor and the antivirus effects have been reported in some viruses. In this study, we examined the anti-DENV effects of PF-429242 using all four serotypes of DENV by several primate-derived cell lines. Moreover, emergence of drug-resistant DENV mutants was assessed by sequential passages with the drug. DENV dependency on intracellular lipids during their infection was also evaluated by adding extracellular lipids. The addition of PF-429242 showed suppression of viral propagation in all DENV serotypes. We showed that drug-resistant DENV mutants are unlikely to emerge after five times sequential passages through treatment with PF-429242. Although the levels of intracellular cholesterol and lipid droplets were reduced by PF-429242, viral propagations were not recovered by addition of exogenous cholesterol or fatty acids, indicating that the reduction of LD and cholesterol caused by PF-429242 treatment is not related to its mechanism of action against DENV propagation. Our results suggest that PF-429242 is a promising candidate for an anti-DENV agent.
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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.