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Cited by 337Herpesvirus Infections and TreatmentsCytomegalovirus and herpesvirus researchVirology and Viral Diseases

Herpes simplex virus glycoproteins E and I facilitate cell-to-cell spread in vivo and across junctions of cultured cells

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Dingwell, K S, Brunetti, C R, Hendricks, R L, Tang, Q, Tang, M, Rainbow, A J, Johnson, D C·1994·Journal of Virology
DOI 10.1128/jvi.68.2.834-845.1994PMC PMC236520
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Abstract

Herpes simplex virus (HSV) glycoproteins E and I (gE and gI) can act as a receptor for the Fc domain of immunoglobulin G (IgG). To examine the role of HSV IgG Fc receptor in viral pathogenesis, rabbits and mice were infected by the corneal route with HSV gE- or gI- mutants. Wild-type HSV-1 produced large dendritic lesions in the corneal epithelium and subsequent stromal disease leading to viral encephalitis, whereas gE- and gI- mutant viruses produced microscopic punctate or small dendritic lesions in the epithelium and no corneal disease or encephalitis. These differences were not related to the ability of the gE-gI oligomer to bind IgG because the differences were observed before the appearance of anti-HSV IgG and in mice, in which IgG binds to the Fc receptor poorly or not at all. Mutant viruses produced small plaques on monolayers of normal human fibroblasts and epithelial cells. Replication of gE- and gI- mutant viruses in human fibroblasts were normal, and the rates of entry of mutant and wild-type viruses into fibroblasts were similar; however, spread of gE- and gI- mutant viruses from cell to cell was significantly slower than that of wild-type HSV-1. In experiments in which fibroblast monolayers were infected with low multiplicities of virus and multiple rounds of infection occurred, the presence of neutralizing antibodies in the culture medium caused the yields of mutant viruses to drop dramatically, whereas there was a lesser effect on the production of wild-type HSV. It appears that cell-to-cell transmission of wild-type HSV-1 occurs by at least two mechanisms: (i) release of virus from cells and entry of extracellular virus into a neighboring cell and (ii) transfer of virus across cell junctions in a manner resistant to neutralizing antibodies. Our results suggest that gE- and gI- mutants are defective in the latter mechanism of spread, suggesting the possibility that the gE-gI complex facilitates virus transfer across cell junctions, a mode of spread which may predominate in some tissues. It is ironic that the gE-gI complex, usually considered an IgG Fc receptor, may, through its ability to mediate cell-to-cell spread, actually protect HSV from IgG in a manner different than previously thought.

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Authors
Dingwell, K. S., Brunetti, C. R., Hendricks, R. L., Tang, Q., Tang, M., Rainbow, A. J., & Johnson, D. C.
Affiliations
McMaster University (CA)
ORCID
Venue
Journal of Virology
Publisher
American Society for Microbiology
Published
1994-02
Volume
68
Issue
2
Pages
834-845
ISSN
  • 0022-538X (ISSN-L)
  • 1098-5514
DOI
10.1128/jvi.68.2.834-845.1994
PMC
PMC236520
OpenAlex
W2169191388
Cited by
337
References
64
Citations by year
2026: 3 · 2025: 4 · 2024: 3 · 2023: 8 · 2022: 7 · 2021: 7 · 2020: 8 · 2019: 10 · 2018: 11 · 2017: 6 · 2016: 8 · 2015: 8 · 2014: 12 · 2013: 8 · 2012: 6
FWCI
13.71
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Journal of Virology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
  • Health Sciences › Medicine › Epidemiology › Cytomegalovirus and herpesvirus research
  • Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
Keywords
herpes simplex virus type 1, glycoprotein E, glycoprotein I, cell-to-cell transmission, IgG Fc receptor, corneal infection, viral encephalitis, cell junctions, neutralizing antibodies, viral pathogenesis, fibroblasts, epithelial cells
MeSH terms
Animals, Biological Transport, Cell Communication, Cells, Cultured, Female, Fibroblasts, Humans, Intercellular Junctions, Viral Plaque Assay, Receptors, Fc, Viral Envelope Proteins, Virulence, Mutagenesis, Herpesvirus 1, Human, Mice

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