Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
J Virol. 2014 Mar;88(6):3591-7. doi: 10.1128/JVI.03081-13. Epub 2013 Dec 26.
The ORF75c tegument protein of murine gammaherpesvirus 68 (MHV68) promotes the degradation of the antiviral promyelocytic leukemia (PML) protein. Surprisingly, MHV68 expressing a degradation-deficient ORF75c replicated in cell culture and in mice similar to the wild-type virus. However, in cells infected with this mutant virus, PML formed novel track-like structures that are induced by ORF61, the viral ribonucleotide reductase large subunit. These findings may explain why ORF75c mutant viruses unable to degrade PML had no demonstrable phenotype after infection.
鼠γ疱疹病毒 68(MHV68)的 ORF75c 衣壳蛋白促进抗病毒早幼粒细胞白血病(PML)蛋白的降解。令人惊讶的是,表达一种降解缺陷的 ORF75c 的 MHV68 在细胞培养中和在小鼠中复制的情况与野生型病毒相似。然而,在感染这种突变病毒的细胞中,PML 形成了由病毒核糖核苷酸还原酶大亚基 ORF61 诱导的新型轨道样结构。这些发现可能解释了为什么不能降解 PML 的 ORF75c 突变病毒在感染后没有表现出明显的表型。