ArticleScience translational medicine2025
Eliminating interactions with the viral Fc receptor improves antibody-mediated protection against neonatal HSV infection in mice.
Article in Science translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- Human herpesvirus evasion of humoral immunity and implications for vaccine development.Nature reviews. Microbiology · 2026Review
- Antibodies targeting HSV glycoprotein B require effector functions to protect neonatal mice.Journal of virology · 2026Article
- Progress and prospects for herpesvirus vaccination using gB antigens.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
- Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- A New Era in Oncology: Clinical Insights Into the Application of Oncolytic Viruses.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
- Update of
Authors and funding
10 authors.
Funding
Abstract
Herpes simplex virus (HSV) encodes surface glycoproteins that are host defense evasion molecules. For example, glycoproteins E and I (gE/gI) form a viral Fc receptor (vFcR) for most subclasses and allotypes of human IgG, promoting evasion of humoral immune responses. Although monoclonal antibodies (mAbs) protect mice from neonatal HSV (nHSV) infections, the impact of vFcR activity on mAb-mediated protection is unknown. Using HSV-1 with intact and ablated gE-mediated Fc binding, as well as Fc-engineered mAbs with modified ability to interact with gE/gI, we investigated the role of the vFcR in mAb-mediated protection from nHSV. HSV-specific mAbs modified to lack binding to gE exhibited enhanced neutralization in vitro and superior protection in vivo compared with their native IgG1 forms. Improved protection was dependent on the presence of vFcR activity and was observed for mAbs specific for both glycoprotein D and glycoprotein B, as well as for a nonneutralizing mAb, and for both laboratory-adapted and clinical isolates of HSV-1 and HSV-2. Further, human IgG3 allotypes, including those lacking vFcR binding, also exhibited enhanced antiviral activity in vivo, identifying a unique viral susceptibility to this subclass. In summary, this study demonstrates that rendering mAbs insensitive to the vFcR can improve protection against HSV, offering prospects for antibody-based interventions.
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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.