Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells

Lilly Cheng Immergluck, Miriam S. Domowicz, Nancy B. Schwartz, Betsy Herold

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Herpes simplex virus (HSV) causes many disease states including mucosal lesions, encephalitis or disseminated infection in the immunocompromised host. These diverse clinical manifestations reflect the capacity of the virus to infect both epithelial and neuronal cell types. Determining the requirements for virus entry into both cell types may provide insights into the pathogenesis of HSV. Previous studies have focused on identifying viral and cellular requirements for entry using epithelial cells. However, little is known about the requirements for binding and entry into neuronal cells. The purpose of the studies reported here was to identify viral and cellular components involved in entry of HSV-1 into primary neuronal cells. Heparan sulfate glycosaminoglycans were found to serve as a receptor for entry of HSV-1 into primary neuronal cells. Evidence to support this includes the findings that heparin (an analogue of heparan sulfate) competitively inhibited virus binding and expression of immediate early virus gene products. In addition, heparitinase removed viral receptors and inhibited virus entry. In epithelial cells, deletion of HSV-1 glycoprotein C (gC) results in virions that have reduced specific binding activity (virus particles bound per cell) and specific infectivity. However, in neuronal cells, it was found that deletion of gC resulted in no loss in specific binding activity, but did result in significant impairment of virus entry as measured by expression of immediate early viral gene product. Taken together, these findings suggest cell-type differences in virus binding and entry and a different role for gC in neuronal cell infection.

Original languageEnglish (US)
Pages (from-to)549-559
Number of pages11
JournalJournal of General Virology
Volume79
Issue number3
StatePublished - Mar 1998
Externally publishedYes

Fingerprint

Human Herpesvirus 1
Virus Internalization
Virus Attachment
Immediate-Early Genes
Heparitin Sulfate
Epithelial Cells
Simplexvirus
heparitinsulfate lyase
Virion
Viruses
Viral Structures
Immunocompromised Host
Viral Proteins
Encephalitis
Infection
Glycosaminoglycans
Heparin
glycoprotein gC, herpes simplex virus type 1

ASJC Scopus subject areas

  • Virology
  • Immunology

Cite this

Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells. / Immergluck, Lilly Cheng; Domowicz, Miriam S.; Schwartz, Nancy B.; Herold, Betsy.

In: Journal of General Virology, Vol. 79, No. 3, 03.1998, p. 549-559.

Research output: Contribution to journalArticle

Immergluck, Lilly Cheng ; Domowicz, Miriam S. ; Schwartz, Nancy B. ; Herold, Betsy. / Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells. In: Journal of General Virology. 1998 ; Vol. 79, No. 3. pp. 549-559.
@article{736c50bc20f34fb9a42f87290a2de1ec,
title = "Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells",
abstract = "Herpes simplex virus (HSV) causes many disease states including mucosal lesions, encephalitis or disseminated infection in the immunocompromised host. These diverse clinical manifestations reflect the capacity of the virus to infect both epithelial and neuronal cell types. Determining the requirements for virus entry into both cell types may provide insights into the pathogenesis of HSV. Previous studies have focused on identifying viral and cellular requirements for entry using epithelial cells. However, little is known about the requirements for binding and entry into neuronal cells. The purpose of the studies reported here was to identify viral and cellular components involved in entry of HSV-1 into primary neuronal cells. Heparan sulfate glycosaminoglycans were found to serve as a receptor for entry of HSV-1 into primary neuronal cells. Evidence to support this includes the findings that heparin (an analogue of heparan sulfate) competitively inhibited virus binding and expression of immediate early virus gene products. In addition, heparitinase removed viral receptors and inhibited virus entry. In epithelial cells, deletion of HSV-1 glycoprotein C (gC) results in virions that have reduced specific binding activity (virus particles bound per cell) and specific infectivity. However, in neuronal cells, it was found that deletion of gC resulted in no loss in specific binding activity, but did result in significant impairment of virus entry as measured by expression of immediate early viral gene product. Taken together, these findings suggest cell-type differences in virus binding and entry and a different role for gC in neuronal cell infection.",
author = "Immergluck, {Lilly Cheng} and Domowicz, {Miriam S.} and Schwartz, {Nancy B.} and Betsy Herold",
year = "1998",
month = "3",
language = "English (US)",
volume = "79",
pages = "549--559",
journal = "Journal of General Virology",
issn = "0022-1317",
publisher = "Society for General Microbiology",
number = "3",

}

TY - JOUR

T1 - Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells

AU - Immergluck, Lilly Cheng

AU - Domowicz, Miriam S.

AU - Schwartz, Nancy B.

AU - Herold, Betsy

PY - 1998/3

Y1 - 1998/3

N2 - Herpes simplex virus (HSV) causes many disease states including mucosal lesions, encephalitis or disseminated infection in the immunocompromised host. These diverse clinical manifestations reflect the capacity of the virus to infect both epithelial and neuronal cell types. Determining the requirements for virus entry into both cell types may provide insights into the pathogenesis of HSV. Previous studies have focused on identifying viral and cellular requirements for entry using epithelial cells. However, little is known about the requirements for binding and entry into neuronal cells. The purpose of the studies reported here was to identify viral and cellular components involved in entry of HSV-1 into primary neuronal cells. Heparan sulfate glycosaminoglycans were found to serve as a receptor for entry of HSV-1 into primary neuronal cells. Evidence to support this includes the findings that heparin (an analogue of heparan sulfate) competitively inhibited virus binding and expression of immediate early virus gene products. In addition, heparitinase removed viral receptors and inhibited virus entry. In epithelial cells, deletion of HSV-1 glycoprotein C (gC) results in virions that have reduced specific binding activity (virus particles bound per cell) and specific infectivity. However, in neuronal cells, it was found that deletion of gC resulted in no loss in specific binding activity, but did result in significant impairment of virus entry as measured by expression of immediate early viral gene product. Taken together, these findings suggest cell-type differences in virus binding and entry and a different role for gC in neuronal cell infection.

AB - Herpes simplex virus (HSV) causes many disease states including mucosal lesions, encephalitis or disseminated infection in the immunocompromised host. These diverse clinical manifestations reflect the capacity of the virus to infect both epithelial and neuronal cell types. Determining the requirements for virus entry into both cell types may provide insights into the pathogenesis of HSV. Previous studies have focused on identifying viral and cellular requirements for entry using epithelial cells. However, little is known about the requirements for binding and entry into neuronal cells. The purpose of the studies reported here was to identify viral and cellular components involved in entry of HSV-1 into primary neuronal cells. Heparan sulfate glycosaminoglycans were found to serve as a receptor for entry of HSV-1 into primary neuronal cells. Evidence to support this includes the findings that heparin (an analogue of heparan sulfate) competitively inhibited virus binding and expression of immediate early virus gene products. In addition, heparitinase removed viral receptors and inhibited virus entry. In epithelial cells, deletion of HSV-1 glycoprotein C (gC) results in virions that have reduced specific binding activity (virus particles bound per cell) and specific infectivity. However, in neuronal cells, it was found that deletion of gC resulted in no loss in specific binding activity, but did result in significant impairment of virus entry as measured by expression of immediate early viral gene product. Taken together, these findings suggest cell-type differences in virus binding and entry and a different role for gC in neuronal cell infection.

UR - http://www.scopus.com/inward/record.url?scp=0031881509&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031881509&partnerID=8YFLogxK

M3 - Article

VL - 79

SP - 549

EP - 559

JO - Journal of General Virology

JF - Journal of General Virology

SN - 0022-1317

IS - 3

ER -