ReviewFrontiers in cellular and infection microbiology2019
Herpes Simplex Virus Evasion of Early Host Antiviral Responses.
Review in Frontiers in cellular and infection microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.
- Pooled it
- In vivo topical gene therapy for recessive dystrophic epidermolysis bullosa: a phase 1 and 2 trial.Nature medicine · 2022Trial
- The cell-type-specific roles of Toll-like receptors in herpes simplex virus infection and pathogenesis.Virulence · 2026Review
- Review
- Host Genetic Susceptibility and Antiviral Immunity Shape the Pathogenesis and Outcomes of Herpes Simplex Encephalitis.Biology · 2026Review
- Article
- Virus reactivation in acute and long COVID-19.Nature · 2026Article
- Immunomodulatory role and therapeutic potential of thrombospondin-1 during infectious diseases and autoimmunity.BMC biology · 2026Review
- Host Immune Response Mechanisms Against Herpes Simplex Virus Type 2 Infection.Pathogens (Basel, Switzerland) · 2026Review
- Z-DNA binding protein 1 mediates necroptotic cell death in primary murine microglia following herpes simplex virus-1 infection.Journal of neurovirology · 2026Article
- Association between dietary zinc intake and herpes simplex virus seropositivity in U.S. adults: a cross-sectional study.BMC infectious diseases · 2026Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025Article
- Hexokinase-2 as a Therapeutic Target: Alleviating Herpes Simplex Keratitis Through Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Extracellular Vesicles Containing MDP Derived from Lactobacillus rhamnosus GG Inhibit HSV-2 Infection by Activating the NOD2-IFN-I Signalling Pathway.Journal of extracellular vesicles · 2025Article
- Small molecule UCM05 inhibits HSV-2 infection via targeting viral glycoproteins and fatty acid synthase with potentiating antiviral immunity.Virology journal · 2025Article
- Modeling Virus-Associated Central Nervous System Disease in Non-Human Primates.International journal of molecular sciences · 2025Review
- Serotype-specific host proteome remodeling in human foreskin fibroblasts during lytic HSV-1 and HSV-2 infection.Virology journal · 2025Article
- Article
- A microengineered 3D human neurovascular unit model to probe the neuropathogenesis of herpes simplex encephalitis.Nature communications · 2025Article
31 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2) have co-evolved with humans for thousands of years and are present at a high prevalence in the population worldwide. HSV infections are responsible for several illnesses including skin and mucosal lesions, blindness and even life-threatening encephalitis in both, immunocompetent and immunocompromised individuals of all ages. Therefore, diseases caused by HSVs represent significant public health burdens. Similar to other herpesviruses, HSV-1 and HSV-2 produce lifelong infections in the host by establishing latency in neurons and sporadically reactivating from these cells, eliciting recurrences that are accompanied by viral shedding in both, symptomatic and asymptomatic individuals. The ability of HSVs to persist and recur in otherwise healthy individuals is likely given by the numerous virulence factors that these viruses have evolved to evade host antiviral responses. Here, we review and discuss molecular mechanisms used by HSVs to evade early innate antiviral responses, which are the first lines of defense against these viruses. A comprehensive understanding of how HSVs evade host early antiviral responses could contribute to the development of novel therapies and vaccines to counteract these viruses.
Indexed as
Identifiers
What Socratic 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 Socratic graph.