Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, The Netherlands.
Virology. 2011 Feb 5;410(1):192-200. doi: 10.1016/j.virol.2010.10.040. Epub 2010 Dec 4.
In human adenoviruses (HAdV), 240 copies of the 14.3-kDa minor capsid protein IX stabilize the capsid. Three N-terminal domains of protein IX form triskelions between hexon capsomers. The C-terminal domains of four protein IX monomers associate near the facet periphery. The precise biological role of protein IX remains enigmatic. Here we show that deletion of the protein IX gene from a HAdV-5 vector enhanced the reporter gene delivery 5 to 25-fold, specifically to Coxsackie and Adenovirus Receptor (CAR)-negative cell lines. Deletion of the protein IX gene also resulted in enhanced activation of peripheral blood mononuclear cells. The mechanism for the enhanced transduction is obscure. No differences in fiber loading, integrin-dependency of transduction, or factor-X binding could be established between protein IX-containing and protein IX-deficient particles. Our data suggest that protein IX can affect the cell tropism of HAdV-5, and may function to dampen the innate immune responses against HAdV particles.
在人类腺病毒（HAdV）中，240 个 14.3kDa 的次要衣壳蛋白 IX 稳定衣壳。蛋白 IX 的三个 N 端结构域在六邻体衣壳之间形成三臂轮。四个蛋白 IX 单体的 C 端结构域在小面周边附近结合。蛋白 IX 的精确生物学作用仍然是个谜。在这里，我们表明，从 HAdV-5 载体中删除蛋白 IX 基因可使报告基因的转导增强 5 至 25 倍，特别是针对柯萨奇病毒和腺病毒受体（CAR）阴性细胞系。删除蛋白 IX 基因还导致外周血单核细胞的激活增强。增强转导的机制尚不清楚。在含有蛋白 IX 和缺乏蛋白 IX 的颗粒之间，纤维装载、转导对整合素的依赖性或因子 X 结合均无差异。我们的数据表明，蛋白 IX 可以影响 HAdV-5 的细胞嗜性，并且可能起作用以抑制针对 HAdV 颗粒的先天免疫反应。
