ArticlePLoS pathogens2015
Secreted herpes simplex virus-2 glycoprotein G modifies NGF-TrkA signaling to attract free nerve endings to the site of infection.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Glycoprotein G enables HSV-2 neuroinvasion and provides protection as a glycosylated vaccine antigen.PLoS pathogens · 2026Article
- HSPA5, a Host Cellular Heat-Shock Protein Required for Influenza a Virus Replication.International journal of molecular sciences · 2025Article
- A review of HSV pathogenesis, vaccine development, and advanced applications.Molecular biomedicine · 2024Review
- Article
- Association between human herpes simplex virus and severe headache or migraine among aged 20-49 years: a cross-sectional study.Frontiers in neurology · 2024Article
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- Effective therapeutic strategies in a preclinical mouse model of Charcot-Marie-Tooth disease.Human molecular genetics · 2021Article
- Tissue-Resident-Memory CD8Frontiers in immunology · 2021Article
- Identification of the Cleavage Domain within Glycoprotein G of Herpes Simplex Virus Type 2.Viruses · 2020Article
- Herpes Simplex Virus 2 Counteracts Neurite Outgrowth Repulsion during Infection in a Nerve Growth Factor-Dependent Manner.Journal of virology · 2020Article
- Olfactory sensory neurons mediate ultrarapid antiviral immune responses in a TrkA-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Neuronal Subtype Determines Herpes Simplex Virus 1 Latency-Associated-Transcript Promoter Activity during Latency.Journal of virology · 2018Article
- Keratinocytes produce IL-17c to protect peripheral nervous systems during human HSV-2 reactivation.The Journal of experimental medicine · 2017Article
- Isolation, Purification, and Culture of Primary Murine Sensory Neurons.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Technologies for Proteome-Wide Discovery of Extracellular Host-Pathogen Interactions.Journal of immunology research · 2017Review
- Secreted herpes simplex virus-2 glycoprotein G alters thermal pain sensitivity by modifying NGF effects on TRPV1.Journal of neuroinflammation · 2016Article
- Viruses exploit the tissue physiology of the host to spread in vivo.Current opinion in cell biology · 2016Review
- Vaccination with the Secreted Glycoprotein G of Herpes Simplex Virus 2 Induces Protective Immunity after Genital Infection.Viruses · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus type 1 (HSV-1) and HSV-2 are highly prevalent viruses that cause a variety of diseases, from cold sores to encephalitis. Both viruses establish latency in peripheral neurons but the molecular mechanisms facilitating the infection of neurons are not fully understood. Using surface plasmon resonance and crosslinking assays, we show that glycoprotein G (gG) from HSV-2, known to modulate immune mediators (chemokines), also interacts with neurotrophic factors, with high affinity. In our experimental model, HSV-2 secreted gG (SgG2) increases nerve growth factor (NGF)-dependent axonal growth of sympathetic neurons ex vivo, and modifies tropomyosin related kinase (Trk)A-mediated signaling. SgG2 alters TrkA recruitment to lipid rafts and decreases TrkA internalization. We could show, with microfluidic devices, that SgG2 reduced NGF-induced TrkA retrograde transport. In vivo, both HSV-2 infection and SgG2 expression in mouse hindpaw epidermis enhance axonal growth modifying the termination zone of the NGF-dependent peptidergic free nerve endings. This constitutes, to our knowledge, the discovery of the first viral protein that modulates neurotrophins, an activity that may facilitate HSV-2 infection of neurons. This dual function of the chemokine-binding protein SgG2 uncovers a novel strategy developed by HSV-2 to modulate factors from both the immune and nervous systems.
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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.