ArticleJournal of virology2002
Herpes simplex virus type 1 evades the effects of antibody and complement in vivo.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 106 citations in OpenAlex.
- The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- HSV-2 gE2/gI2 are immune evasion molecules that bind IgG Fc to inhibit antibody-dependent cellular cytotoxicity.Frontiers in immunology · 2026Article
- A fur plucking model to study herpes simplex virus reactivation and recurrent disease.mSphere · 2024Article
- A review of HSV pathogenesis, vaccine development, and advanced applications.Molecular biomedicine · 2024Review
- Viral Factors in Modulation of Host Immune Response: A Route to Novel Antiviral Agents and New Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Safety of non-replicative and oncolytic replication-selective HSV vectors.Trends in molecular medicine · 2024Review
- Review
- Boosting of vaginal HSV-2-specific B and T cell responses by intravaginal therapeutic immunization results in diminished recurrent HSV-2 disease.Journal of virology · 2023Article
- Article
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- B cells join T cell clusters in the host response to recurrent herpes simplex virus 2 infection.The Journal of clinical investigation · 2021Article
- Stunning symmetries involved in the self-assembly of the HSV-1 capsid.The journal of the Korean Physical Society · 2021Review
- Article
- Epstein-Barr Virus and Systemic Autoimmune Diseases.Frontiers in immunology · 2020Review
- Complement and CD4eLife · 2019Article
- Virus envelope tissue factor promotes infection in mice.Journal of thrombosis and haemostasis : JTH · 2019Article
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
- Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses.Scientific reports · 2017Article
- Viral-derived complement inhibitors: current status and potential role in immunomodulation.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Let's Tie the Knot: Marriage of Complement and Adaptive Immunity in Pathogen Evasion, for Better or Worse.Frontiers in microbiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) encodes a complement-interacting glycoprotein, gC, and an immunoglobulin G (IgG) Fc binding glycoprotein, gE, that mediate immune evasion by affecting multiple aspects of innate and acquired immunity, including interfering with complement components C1q, C3, C5, and properdin and blocking antibody-dependent cellular cytotoxicity. Previous studies evaluated the individual contributions of gC and gE to immune evasion. Experiments in a murine model that examines the combined effects of gC and gE immune evasion on pathogenesis are now reported. Virulence of wild-type HSV-1 is compared with mutant viruses defective in gC-mediated C3 binding, gE-mediated IgG Fc binding, or both immune evasion activities. Eliminating both activities greatly increased susceptibility of HSV-1 to antibody and complement neutralization in vitro and markedly reduced virulence in vivo as measured by disease scores, virus titers, and mortality. Studies with C3 knockout mice indicated that other activities attributed to these glycoproteins, such as gC-mediated virus attachment to heparan sulfate or gE-mediated cell-to-cell spread, do not account for the reduced virulence of mutant viruses. The results support the importance of gC and gE immune evasion in vivo and suggest potential new targets for prevention and treatment of HSV disease.
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.