Research at the Klaus Früh Lab
1. Human cytomegalovirus (HCMV)
Human cytomegalovirus (HCMV) infection alters the expression of many cellular genes,
including interferon stimulated genes (ISGs). Using high density cDNA microarrays we have shown that the HCMV-regulated gene expression profile in fibroblasts does not differ substantially from the response generated by interferon (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 unidentified cellular receptor is the principal mechanism by which HCMV alters cellular gene expression early during infection. These findings highlight a new paradigm for the consequences of virus-receptor interactions
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