Institute for Clinical and Molecular Virology, University of Erlangen-Nuremberg, Schlossgarten 4, 91054 Erlangen, Germany.
Virus Res. 2011 May;157(2):128-33. doi: 10.1016/j.virusres.2010.10.002. Epub 2010 Oct 8.
In recent studies we and others have identified the cellular proteins PML, hDaxx, Sp100 and ATRX, which form a subnuclear structure known as nuclear domain 10 (ND10) or PML nuclear bodies (PML-NBs), as host restriction factors that counteract cytomegalovirus infections by inhibiting the initiation of viral immediate-early (IE) gene expression. The antiviral function of ND10, however, is antagonized by viral regulatory proteins which either induce a proteasomal degradation of ND10 proteins or a disruption of the subnuclear structure. This review will summarize our current knowledge on the inhibition of cytomegalovirus replication by ND10 proteins. Furthermore, viral strategies to defeat this host defense mechanism are discussed.
在最近的研究中，我们和其他人已经确定了细胞蛋白 PML、hDaxx、Sp100 和 ATRX，它们形成了一个亚核结构，称为核域 10（ND10）或 PML 核体（PML-NBs），作为宿主限制因子，通过抑制病毒即刻早期（IE）基因表达的起始来抵抗巨细胞病毒感染。然而，ND10 的抗病毒功能受到病毒调节蛋白的拮抗，这些蛋白要么诱导 ND10 蛋白的蛋白酶体降解，要么破坏亚核结构。这篇综述将总结我们目前对 ND10 蛋白抑制巨细胞病毒复制的认识。此外，还讨论了病毒击败这种宿主防御机制的策略。
