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Sci Rep. 2017 Jan 3;7:39861. doi: 10.1038/srep39861.

CTCF interacts with the lytic HSV-1 genome to promote viral transcription.

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Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences &Yunnan Province, Kunming Institute of Zoology, Kunming, Kunming 650223, China.
Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, Beijing 100101, China.
Gene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Biology &Chemistry Engineering College, Panzhihua University, Panzhihua, Sichuan 617000, China.
Department of Biology, Arcadia University, Glenside, PA 19038, USA.
Institutes of Biology and Medical Sciences, Soochow University, Suzhou, 215123, China.
Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, AB T2N 4N1, Canada.
Department of Viral Immunology, Institute of Medical Biology, Chinese Academy of Medicine Science, Peking Union Medical College, Kunming, Kunming 650118, China.
Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.


CTCF is an essential chromatin regulator implicated in important nuclear processes including in nuclear organization and transcription. Herpes Simplex Virus-1 (HSV-1) is a ubiquitous human pathogen, which enters productive infection in human epithelial and many other cell types. CTCF is known to bind several sites in the HSV-1 genome during latency and reactivation, but its function has not been defined. Here, we report that CTCF interacts extensively with the HSV-1 DNA during lytic infection by ChIP-seq, and its knockdown results in the reduction of viral transcription, viral genome copy number and virus yield. CTCF knockdown led to increased H3K9me3 and H3K27me3, and a reduction of RNA pol II occupancy on viral genes. Importantly, ChIP-seq analysis revealed that there is a higher level of CTD Ser2P modified RNA Pol II near CTCF peaks relative to the Ser5P form in the viral genome. Consistent with this, CTCF knockdown reduced the Ser2P but increased Ser5P modified forms of RNA Pol II on viral genes. These results suggest that CTCF promotes HSV-1 lytic transcription by facilitating the elongation of RNA Pol II and preventing silenced chromatin on the viral genome.

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