ArticleJournal of innate immunity2009
Toll-like receptor 2 senses hepatitis C virus core protein but not infectious viral particles.
Article in Journal of innate immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Viruses Binding to Host Receptors Interacts with Autophagy.International journal of molecular sciences · 2023Review
- Controlling viral inflammatory lesions by rebalancing immune response patterns.Frontiers in immunology · 2023Review
- Scratching the Surface Takes a Toll: Immune Recognition of Viral Proteins by Surface Toll-like Receptors.Viruses · 2022Review
- Toll-like Receptor Response to Hepatitis C Virus Infection: A Recent Overview.International journal of molecular sciences · 2022Review
- Swine Enteric Coronavirus: Diverse Pathogen-Host Interactions.International journal of molecular sciences · 2022Review
- Review
- Crosstalk Between Intestinal Serotonergic System and Pattern Recognition Receptors on the Microbiota-Gut-Brain Axis.Frontiers in endocrinology · 2021Review
- Toll-like receptor-2 exacerbates murine acute viral hepatitis.Immunology · 2016Article
- Human Coronaviruses: A Review of Virus-Host Interactions.Diseases (Basel, Switzerland) · 2016Review
- Review
- Hepatitis C, innate immunity and alcohol: friends or foes?Biomolecules · 2015Review
- Hepatitis C virus core protein enhances HIV-1 replication in human macrophages through TLR2, JNK, and MEK1/2-dependent upregulation of TNF-α and IL-6.FEBS letters · 2014Article
- Identification of hepatitis C virus inhibitors targeting different aspects of infection using a cell-based assay.Antimicrobial agents and chemotherapy · 2012Article
- Sensing of RNA viruses: a review of innate immune receptors involved in recognizing RNA virus invasion.Journal of virology · 2012Review
- Dendritic cells in hepatitis C infection: can they (help) win the battle?Journal of gastroenterology · 2011Review
- Hepatitis C virus core protein: Not just a nucleocapsid building block, but an immunity and inflammation modulator.Tzu chi medical journalReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are pathogen recognition molecules activating the innate immune system. Cell surface expressed TLRs, such as TLR2 and TLR4, have been shown to play an important role in human host defenses against viruses through sensing of viral structural proteins. In this study, we aimed to elucidate whether TLR2 and TLR4 participate in inducing antiviral immunity against hepatitis C virus (HCV) by sensing viral structural proteins. We studied TLR2 and TLR4 activation by cell culture-derived infectious virions and serum-derived virions in comparison to purified recombinant HCV structural proteins and enveloped virus-like particles. Incubation of TLR2 or TLR4 transfected cell lines with recombinant core protein resulted in activation of TLR2-dependent signaling. In contrast, neither infectious virions nor enveloped HCV-like particles triggered TLR2 and TLR4 signaling. These findings suggest that monomeric HCV core protein but not intact infectious particles are sensed by TLR2. Impairment of interaction between TLR and the core in infectious viral particles may contribute to escape from innate antiviral immune responses.
Indexed as
Identifiers
What OpenQuestion holds
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.