ArticlePLoS neglected tropical diseases2012
G protein-coupled receptor kinase 2 promotes flaviviridae entry and replication.
Article in PLoS neglected tropical diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 79 citations in OpenAlex.
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- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- A No-Brainer! The Therapeutic Potential of TRIM Proteins in Viral and Central Nervous System Diseases.Viruses · 2025Review
- Pathogenesis and clinical management of arboviral diseases.World journal of virology · 2025Review
- Machine learning-based gene expression biomarkers to distinguish Zika and Dengue virus infections: implications for diagnosis.Virusdisease · 2024Article
- Multiple receptor tyrosine kinases regulate dengue infection of hepatocytes.Frontiers in cellular and infection microbiology · 2024Article
- Article
- CMPK2 restricts Zika virus replication by inhibiting viral translation.PLoS pathogens · 2023Article
- Targeting Human Proteins for Antiviral Drug Discovery and Repurposing Efforts: A Focus on Protein Kinases.Viruses · 2023Review
- β-arrestins and G protein-coupled receptor kinases in viral entry: A graphical review.Cellular signalling · 2023Review
- Review
- Fatal attraction: The roles of ribosomal proteins in the viral life cycle.Wiley interdisciplinary reviews. RNA · 2021Review
- Review
- Iminosugars: A host-targeted approach to combat Flaviviridae infections.Antiviral research · 2020Review
- Dengue virus induces PCSK9 expression to alter antiviral responses and disease outcomes.The Journal of clinical investigation · 2020Article
- Topoisomerase III-β is required for efficient replication of positive-sense RNA viruses.Antiviral research · 2020Article
- Squaring the EMC - how promoting membrane protein biogenesis impacts cellular functions and organismal homeostasis.Journal of cell science · 2020Review
- Topoisomerase III-ß is required for efficient replication of positive-sense RNA viruses.bioRxiv : the preprint server for biology · 2020Article
- To TRIM or not to TRIM: the balance of host-virus interactions mediated by the ubiquitin system.The Journal of general virology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Flaviviruses cause a wide range of severe diseases ranging from encephalitis to hemorrhagic fever. Discovery of host factors that regulate the fate of flaviviruses in infected cells could provide insight into the molecular mechanisms of infection and therefore facilitate the development of anti-flaviviral drugs. We performed genome-scale siRNA screens to discover human host factors required for yellow fever virus (YFV) propagation. Using a 2 × 2 siRNA pool screening format and a duplicate of the screen, we identified a high confidence list of YFV host factors. To find commonalities between flaviviruses, these candidates were compared to host factors previously identified for West Nile virus (WNV) and dengue virus (DENV). This comparison highlighted a potential requirement for the G protein-coupled receptor kinase family, GRKs, for flaviviral infection. The YFV host candidate GRK2 (also known as ADRBK1) was validated both in siRNA-mediated knockdown HuH-7 cells and in GRK(-/-) mouse embryonic fibroblasts. Additionally, we showed that GRK2 was required for efficient propagation of DENV and Hepatitis C virus (HCV) indicating that GRK2 requirement is conserved throughout the Flaviviridae. Finally, we found that GRK2 participates in multiple distinct steps of the flavivirus life cycle by promoting both entry and RNA synthesis. Together, our findings identified GRK2 as a novel regulator of flavivirus infection and suggest that inhibition of GRK2 function may constitute a new approach for treatment of flavivirus associated diseases.
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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.