ReviewJournal of molecular biology2014
Recognition of herpes simplex viruses: toll-like receptors and beyond.
Review in Journal of molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 108 citations in OpenAlex.
- Higher levels of circulating monocyte-platelet aggregates are correlated with viremia and increased sCD163 levels in HIV-1 infection.Cellular & molecular immunology · 2015Trial
- Inflammatory Cytokine Changes in Herpes Simplex Virus Infected Periodontium: An In Vitro Proteomic Study.Oral diseases · 2026Article
- Nociceptor neurons shape antiviral immunity.Journal of neuroinflammation · 2026Review
- Marine Derived Natural Products: Emerging Therapeutics Against Herpes Simplex Virus Infection.Biomolecules · 2026Review
- The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025Article
- Prevalence of HSV Genomic Signatures Among Acanthamoeba Hosts and Contaminated Lens Cases: A Molecular and Clinical Study.Investigative ophthalmology & visual science · 2025Article
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- An updated review of HSV-1 infection-associated diseases and treatment, vaccine development, and vector therapy application.Virulence · 2024Review
- Review
- Review
- Prunella vulgaris polysaccharide inhibits herpes simplex virus infection by blocking TLR-mediated NF-κB activation.Chinese medicine · 2024Article
- Understanding the Neurotrophic Virus Mechanisms and Their Potential Effect on Systemic Lupus Erythematosus Development.Brain sciences · 2024Review
- IRF7 and UNC93B1 variants in an infant with recurrent herpes simplex virus infection.The Journal of clinical investigation · 2023Article
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- Review
- When herpes simplex virus encephalitis meets antiviral innate immunity.Frontiers in immunology · 2023Review
- Archaic connectivity between the sulfated heparan sulfate and the herpesviruses - An evolutionary potential for cross-species interactions.Computational and structural biotechnology journal · 2023Review
- TLR9 and Glioma: Friends or Foes?Cells · 2022Review
- Review
6 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
Herpes simplex viruses (HSVs) are human pathogens that establish lytic and latent infections. Reactivation from latency occurs intermittently, which represents a lifelong source of recurrent infection. In this complex process, HSV triggers and neutralizes innate immunity. Therefore, a dynamic equilibrium between HSV and the innate immune system determines the outcome of viral infection. Detection of HSV involves pathogen recognition receptors that include Toll-like receptors, retinoic acid-inducible gene I-like receptors, and cytosolic DNA sensors. Moreover, innate components or pathways exist to sense membrane fusion upon viral entry into host cells. Consequently, this surveillance network activates downstream transcription factors, leading to the induction of type I interferon and inflammatory cytokines. Not surprisingly, with the capacity to establish chronic infection HSV has evolved strategies that modulate or evade innate immunity. In this review, we describe recent advances pertinent to the interplay of HSV and the induction of innate immunity mediated by pathogen recognition receptors or pathways.
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.