Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B

Kenneth A. Simmen, Jasbir Singh, B. G Mattias Luukkonen, Matt Lopper, Anton Bittner, Nancy E. Miller, Michael R. Jackson, Teresa Compton, Klaus Frueh

Research output: Contribution to journalArticle

177 Citations (Scopus)

Abstract

Human cytomegalovirus (HCMV) infection alters the expression of many cellular genes, including IFN-stimulated genes (ISGs) [Zhu, H., Cong, J.-P., Mamtora, G., Gingeras, T. & Shenk, T. (1998) Proc. Natl. Acad. Sci. USA 95, 14470-14475]. By using high-density cDNA microarrays, we show that the HCMV-regulated gene expression profile in fibroblasts does not differ substantially from the response generated by IFN. Furthermore, we identified the specific viral component triggering this response as the envelope glycoprotein B (gB). Cells treated with gB, but not other herpesviral glycoproteins, exhibited the same transcriptional profile as HCMV-infected cells. Thus, the interaction of gB with its as yet unidentified cellular receptor is the principal mechanism by which HCMV alters cellular gene expression early during infection. These findings highlight a pioneering paradigm for the consequences of virus-receptor interactions.

Original languageEnglish (US)
Pages (from-to)7140-7145
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume98
Issue number13
DOIs
StatePublished - Jun 19 2001

Fingerprint

Cytomegalovirus
Glycoproteins
Virus Receptors
Viral Structures
Cytomegalovirus Infections
Oligonucleotide Array Sequence Analysis
Transcriptome
Genes
Fibroblasts
Gene Expression
Infection

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B. / Simmen, Kenneth A.; Singh, Jasbir; Luukkonen, B. G Mattias; Lopper, Matt; Bittner, Anton; Miller, Nancy E.; Jackson, Michael R.; Compton, Teresa; Frueh, Klaus.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 98, No. 13, 19.06.2001, p. 7140-7145.

Research output: Contribution to journalArticle

Simmen, Kenneth A. ; Singh, Jasbir ; Luukkonen, B. G Mattias ; Lopper, Matt ; Bittner, Anton ; Miller, Nancy E. ; Jackson, Michael R. ; Compton, Teresa ; Frueh, Klaus. / Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B. In: Proceedings of the National Academy of Sciences of the United States of America. 2001 ; Vol. 98, No. 13. pp. 7140-7145.
@article{d62ae1da305f4779869c6f487574ce09,
title = "Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B",
abstract = "Human cytomegalovirus (HCMV) infection alters the expression of many cellular genes, including IFN-stimulated genes (ISGs) [Zhu, H., Cong, J.-P., Mamtora, G., Gingeras, T. & Shenk, T. (1998) Proc. Natl. Acad. Sci. USA 95, 14470-14475]. By using high-density cDNA microarrays, we show that the HCMV-regulated gene expression profile in fibroblasts does not differ substantially from the response generated by IFN. Furthermore, we identified the specific viral component triggering this response as the envelope glycoprotein B (gB). Cells treated with gB, but not other herpesviral glycoproteins, exhibited the same transcriptional profile as HCMV-infected cells. Thus, the interaction of gB with its as yet unidentified cellular receptor is the principal mechanism by which HCMV alters cellular gene expression early during infection. These findings highlight a pioneering paradigm for the consequences of virus-receptor interactions.",
author = "Simmen, {Kenneth A.} and Jasbir Singh and Luukkonen, {B. G Mattias} and Matt Lopper and Anton Bittner and Miller, {Nancy E.} and Jackson, {Michael R.} and Teresa Compton and Klaus Frueh",
year = "2001",
month = "6",
day = "19",
doi = "10.1073/pnas.121177598",
language = "English (US)",
volume = "98",
pages = "7140--7145",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "13",

}

TY - JOUR

T1 - Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B

AU - Simmen, Kenneth A.

AU - Singh, Jasbir

AU - Luukkonen, B. G Mattias

AU - Lopper, Matt

AU - Bittner, Anton

AU - Miller, Nancy E.

AU - Jackson, Michael R.

AU - Compton, Teresa

AU - Frueh, Klaus

PY - 2001/6/19

Y1 - 2001/6/19

N2 - Human cytomegalovirus (HCMV) infection alters the expression of many cellular genes, including IFN-stimulated genes (ISGs) [Zhu, H., Cong, J.-P., Mamtora, G., Gingeras, T. & Shenk, T. (1998) Proc. Natl. Acad. Sci. USA 95, 14470-14475]. By using high-density cDNA microarrays, we show that the HCMV-regulated gene expression profile in fibroblasts does not differ substantially from the response generated by IFN. Furthermore, we identified the specific viral component triggering this response as the envelope glycoprotein B (gB). Cells treated with gB, but not other herpesviral glycoproteins, exhibited the same transcriptional profile as HCMV-infected cells. Thus, the interaction of gB with its as yet unidentified cellular receptor is the principal mechanism by which HCMV alters cellular gene expression early during infection. These findings highlight a pioneering paradigm for the consequences of virus-receptor interactions.

AB - Human cytomegalovirus (HCMV) infection alters the expression of many cellular genes, including IFN-stimulated genes (ISGs) [Zhu, H., Cong, J.-P., Mamtora, G., Gingeras, T. & Shenk, T. (1998) Proc. Natl. Acad. Sci. USA 95, 14470-14475]. By using high-density cDNA microarrays, we show that the HCMV-regulated gene expression profile in fibroblasts does not differ substantially from the response generated by IFN. Furthermore, we identified the specific viral component triggering this response as the envelope glycoprotein B (gB). Cells treated with gB, but not other herpesviral glycoproteins, exhibited the same transcriptional profile as HCMV-infected cells. Thus, the interaction of gB with its as yet unidentified cellular receptor is the principal mechanism by which HCMV alters cellular gene expression early during infection. These findings highlight a pioneering paradigm for the consequences of virus-receptor interactions.

UR - http://www.scopus.com/inward/record.url?scp=0035912832&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035912832&partnerID=8YFLogxK

U2 - 10.1073/pnas.121177598

DO - 10.1073/pnas.121177598

M3 - Article

VL - 98

SP - 7140

EP - 7145

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 13

ER -