ArticleJournal of virology2013
Herpes simplex virus 1 tropism for human sensory ganglion neurons in the severe combined immunodeficiency mouse model of neuropathogenesis.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Severe Combined Immunodeficiency-Classification, Microbiology Association and Treatment.Microorganisms · 2023Review
- Innate Immune Signaling and Role of Glial Cells in Herpes Simplex Virus- and Rabies Virus-Induced Encephalitis.Viruses · 2021Review
- Herpes simplex virus 1 evades cellular antiviral response by inducing microRNA-24, which attenuates STING synthesis.PLoS pathogens · 2021Article
- Targeting Host Cellular Factors as a Strategy of Therapeutic Intervention for Herpesvirus Infections.Frontiers in cellular and infection microbiology · 2021Review
- The latency-associated transcript locus of herpes simplex virus 1 is a virulence determinant in human skin.PLoS pathogens · 2020Article
- Could autophagy dysregulation link neurotropic viruses to Alzheimer's disease?Neural regeneration research · 2019Review
- Challenges of gene delivery to the central nervous system and the growing use of biomaterial vectors.Brain research bulletin · 2019Review
- Review
- Mechanisms of Host IFI16, PML, and Daxx Protein Restriction of Herpes Simplex Virus 1 Replication.Journal of virology · 2018Article
- Adult Mouse DRG Explant and Dissociated Cell Models to Investigate Neuroplasticity and Responses to Environmental Insults Including Viral Infection.Journal of visualized experiments : JoVE · 2018Article
- The Fc Domain of Immunoglobulin Is Sufficient to Bridge NK Cells with Virally Infected Cells.Immunity · 2017Article
- The Characteristics of Herpes Simplex Virus Type 1 Infection in Rhesus Macaques and the Associated Pathological Features.Viruses · 2017Article
- CD8+ T Cells Play a Bystander Role in Mice Latently Infected with Herpes Simplex Virus 1.Journal of virology · 2016Article
- Neuronal Subtype and Satellite Cell Tropism Are Determinants of Varicella-Zoster Virus Virulence in Human Dorsal Root Ganglia Xenografts In Vivo.PLoS pathogens · 2015Article
- Establishment of HSV1 latency in immunodeficient mice facilitates efficient in vivo reactivation.PLoS pathogens · 2015Article
- Direct transfer of viral and cellular proteins from varicella-zoster virus-infected non-neuronal cells to human axons.PloS one · 2015Article
- Molecular mechanisms of varicella zoster virus pathogenesis.Nature reviews. Microbiology · 2014Review
- Detection of the genome and transcripts of a persistent DNA virus in neuronal tissues by fluorescent in situ hybridization combined with immunostaining.Journal of visualized experiments : JoVE · 2014Article
- Potential of protein kinase inhibitors for treating herpesvirus-associated disease.Trends in microbiology · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The tropism of herpes simplex virus (HSV-1) for human sensory neurons infected in vivo was examined using dorsal root ganglion (DRG) xenografts maintained in mice with severe combined immunodeficiency (SCID). In contrast to the HSV-1 lytic infectious cycle in vitro, replication of the HSV-1 F strain was restricted in human DRG neurons despite the absence of adaptive immune responses in SCID mice, allowing the establishment of neuronal latency. At 12 days after DRG inoculation, 26.2% of human neurons expressed HSV-1 protein and 13.1% expressed latency-associated transcripts (LAT). Some infected neurons showed cytopathic changes, but HSV-1, unlike varicella-zoster virus (VZV), only rarely infected satellite cells and did not induce fusion of neuronal and satellite cell plasma membranes. Cell-free enveloped HSV-1 virions were observed, indicating productive infection. A recombinant HSV-1-expressing luciferase exhibited less virulence than HSV-1 F in the SCID mouse host, enabling analysis of infection in human DRG xenografts for a 61-day interval. At 12 days after inoculation, 4.2% of neurons expressed HSV-1 proteins; frequencies increased to 32.1% at 33 days but declined to 20.8% by 61 days. Frequencies of LAT-positive neurons were 1.2% at 12 days and increased to 40.2% at 33 days. LAT expression remained at 37% at 61 days, in contrast to the decline in neurons expressing viral proteins. These observations show that the progression of HSV-1 infection is highly restricted in human DRG, and HSV-1 genome silencing occurs in human neurons infected in vivo as a consequence of virus-host cell interactions and does not require adaptive immune control.
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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.