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Human cytomegalovirus induces and exploits Roquin to counteract the IRF1-mediated antiviral state
- Human cytomegalovirus induces and exploits Roquin to counteract the IRF1-mediated antiviral state
- Song, Jaewon; Lee, Sanghyun; Cho, Dong-Yeon; Lee, Sungwon; Kim, Hyewon; Yu, Namhee; Lee, Sanghyuk; Ahn, Kwangseog
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA vol. 116, no. 37, pp. 18619 - 18628
- human cytomegalovirus; RNA-binding protein; immune evasion; proinflammatory cytokine
- NATL ACAD SCIENCES
- SCI; SCIE; SCOPUS
- Document Type
- RNA represents a pivotal component of host-pathogen interactions. Human cytomegalovirus (HCMV) infection causes extensive alteration in host RNA metabolism, but the functional relationship between the virus and cellular RNA processing remains largely unknown. Through loss-of-function screening, we show that HCMV requires multiple RNA-processing machineries for efficient viral lytic production. In particular, the cellular RNA-binding protein Roquin, whose expression is actively stimulated by HCMV, plays an essential role in inhibiting the innate immune response. Transcriptome profiling revealed Roquin-dependent global down-regulation of proinflammatory cytokines and antiviral genes in HCMV-infected cells. Furthermore, using cross-linking immunoprecipitation (CLIP)-sequencing (seq), we identified IFN regulatory factor 1 (IRF1), a master transcriptional activator of immune responses, as a Roquin target gene. Roquin reduces IRF1 expression by directly binding to its mRNA, thereby enabling suppression of a variety of antiviral genes. This study demonstrates how HCMV exploits host RNA-binding protein to prevent a cellular antiviral response and offers mechanistic insight into the potential development of CMV therapeutics.
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