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

Proceedings of the National Academy of SciencesPublished 5 June 2001Open access
Kenneth Simmen, Jasbir Singh, B. G. Mattias Luukkonen, Matt Lopper, Anton Bittner, Nancy E. Miller
Citations204
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TL;DR

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, and this findings highlight a pioneering paradigm for the consequences of virus–receptor interactions.

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.

Keywords

Immunology and MicrobiologyMedicine