ArticleJournal of virology2010
Virus-induced Ca2+ influx extends survival of west nile virus-infected cells.
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 49 papers.
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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
49 citing papers in PubMed, 89 citations in OpenAlex.
- Transient receptor potential channels inChannels (Austin, Tex.) · 2026Review
- Disruption of cellular calcium homeostasis by duck Tembusu virus facilitates viral replication via AMPK pathway activation.Frontiers in cellular and infection microbiology · 2026Article
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- Role of Divalent Cations in Infections in Host-Pathogen Interaction.International journal of molecular sciences · 2024Review
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- Engagement of AKT and ERK signaling pathways facilitates infection of human neuronal cells with West Nile virus.Journal of virus eradication · 2024Article
- Sustained antiviral insulin signaling during West Nile virus infection results in viral mutations.Frontiers in cellular and infection microbiology · 2024Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Targeting host calcium channels and viroporins: a promising strategy for SARS-CoV-2 therapy.Future virology · 2023Review
- Interactions of Equine Viruses with the Host Kinase Machinery and Implications for One Health and Human Disease.Viruses · 2023Review
- CaWorld journal of diabetes · 2023Article
- MEK/ERK activation plays a decisive role in Zika virus morphogenesis and release.Archives of virology · 2023Article
- The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Azelnidipine Exhibits In Vitro and In Vivo Antiviral Effects against Flavivirus Infections by Targeting the Viral RdRp.Viruses · 2022Article
- Enhanced CaInternational journal of molecular sciences · 2022Article
- Dihydropyridine-derived calcium channel blocker as a promising anti-hantavirus entry inhibitor.Frontiers in pharmacology · 2022Article
- Berbamine inhibits Japanese encephalitis virus (JEV) infection by compromising TPRMLs-mediated endolysosomal trafficking of low-density lipoprotein receptor (LDLR).Emerging microbes & infections · 2021Article
- Traditional Chinese Medicine and Western Medicine Share Similar Philosophical Approaches to Fight COVID-19.Aging and disease · 2021Article
- Genome-wide identification of Aedes albopictus long noncoding RNAs and their association with dengue and Zika virus infection.PLoS neglected tropical diseases · 2021Article
- Conflicts over calcium and the treatment of COVID-19.Evolution, medicine, and public health · 2021Review
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
Abstract
West Nile virus (WNV) infection leads to rapid and sustained Ca(2+) influx. This influx was observed with different strains of WNV and in different types of cells. Entry during virion endocytosis as well as through calcium channels contributed to the Ca(2+) influx observed in WNV-infected cells. Ca(2+) influx was not detected after infection with vesicular stomatitis virus (VSV) and occurred only through endocytosis in Sindbis virus-infected cells. Caspase 3 cleavage and activation of several kinases, including focal adhesion kinase (FAK), mitogen-activated extracellular signal-regulated protein kinase (ERK1/2), and protein-serine kinase B alpha (Akt), at early times after WNV infection were shown to be dependent on Ca(2+) influx. Although the activation of these kinases was sustained in virus-infected cells throughout infection, UV-inactivated WNV induced only a transient activation of FAK and ERK1/2 at early times after infection. The Ca(2+)-dependent FAK activation observed in WNV-infected cells was not mediated by alphavbeta3 integrins. Reduction of Ca(2+) influx at early times of infection by various treatments decreased the viral yield and delayed both the early transient caspase 3 cleavage and the activation of FAK, Akt, and ERK signaling. The results indicate that Ca(2+) influx is required for early infection events needed for efficient viral replication, possibly for virus-induced rearrangement of the endoplasmic reticulum (ER) membrane. Increased caspase 3 cleavage at both early (transient) and late times of infection correlated with decreased activation of the FAK and ERK1/2 pathways, indicating a role for these kinases in extending the survival of flavivirus-infected cells.
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Registered trials
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