期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：24
页码：14309-14314
DOI：10.1073/pnas.1835673100
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Macrophages (M{phi}) are activated by IFN{gamma} and are important cellular targets for infection by human and murine cytomegalovirus (MCMV), making it advantageous for CMVs to block IFN{gamma}-induced M{phi} differentiation. We found that MCMV infection inhibited IFN{gamma} regulation of many genes in M{phi}. MCMV infection blocked IFN{gamma} responses at the level of transcription without blocking Janus kinase/signal transducer and activator of transcription pathway activation and targeted IFN response factor 1- and class II transactivator-dependent and independent promoters. MCMV did not alter basal transcription from IFN{gamma}-responsive promoters and left the majority of cellular transcripts unchanged even after 48 h of infection. The effects of MCMV infection were specific to chromosomal rather than transiently transfected promoters. Characterization of the IFN{gamma}-responsive chromosomal class II transactivator promoter revealed that MCMV infection blocked IFN{gamma}-induced promoter assembly, allowing the virus to transcriptionally paralyze infected M{phi} responses while allowing basal transcription to proceed.
