CoChat
Sign Up
Cited by 337Herpesvirus Infections and TreatmentsCytomegalovirus and herpesvirus researchVirology and Viral Diseases

The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.

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

Open access
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
Open this paper in CoChat — free account

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.

Overview

Integrity signals

Registry

Crossref · 10.1128/jvi.68.2.834-845.1994

Cites

64 of 64 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

The text we found for this paper looks like another document, so its claims and self-check weren’t run. The registry and citation checks still apply.

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The text we found for this paper looks like another document, so the self-check wasn’t run.

Citations

Cites

Show all 64 references

Cited by

Sorted by citations

Related

See all

Metadata

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 › Infectious Diseases › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review