Bornavirus Closely Associates and Segregates with Host Chromosomes to Ensure Persistent Intranuclear Infection

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• 作者：Yusuke Matsumoto¹ ; ² ; ⁷ ; Yohei Hayashi² ; ⁷ ; ⁸ ; Hiroko Omori³ ; Tomoyuki Honda¹ ; Takuji Daito¹ ; ⁹ ; Masayuki Horie¹ ; ⁴ ; Kazuyoshi Ikuta² ; Kan Fujino¹ ; ² ; Shoko Nakamura¹ ; Urs Schneider⁴ ; Geoffrey Chase⁴ ; Tamotsu Yoshimori⁵ ; Martin Schwemmle⁴ ; Keizo Tomonaga¹ ; ⁶ ; ^{tomonaga@virus.kyoto-u.ac.jp}
• 刊名：Cell Host Microbe
• 出版年：2012
• 期刊代码：P58_19313128
• 类别：imm
• 出版时间：17 May, 2012
• 卷：11
• 期：5
• 页码：492-503
• 文件大小：2188 K

摘要

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Summary

Bornaviruses are nonsegmented negative-strand RNA viruses that establish a persistent infection in the nucleus and occasionally integrate a DNA genome copy into the host chromosomal DNA. However, how these viruses achieve intranuclear infection remains unclear. We show that Borna disease virus (BDV), a mammalian bornavirus, closely associates with the cellular chromosome to ensure intranuclear infection. BDV generates viral factories within the nucleus using host chromatin as a scaffold. In addition, the viral ribonucleoprotein (RNP) interacts directly with the host chromosome throughout the cell cycle, using core histones as a docking platform. HMGB1, a host chromatin-remodeling DNA architectural protein, is required to stabilize RNP on chromosomes and for efficient BDV RNA transcription in the nucleus. During metaphase, the association of RNP with mitotic chromosomes allows the viral RNA to segregate into daughter cells and ensure persistent infection. Thus, bornaviruses likely evolved a chromosome-dependent life cycle to achieve stable intranuclear infection.