Department of Molecular Biosciences, University of Kansas, Lawrence, Kansas 66045, USA.
J Neurovirol. 2010 Oct;16(5):405-9. doi: 10.3109/13550284.2010.513030.
Previous studies have shown that herpes simplex virus type 1 (HSV-1) replication is inhibited by the cyclin-dependent kinase (cdk) inhibitor roscovitine. One roscovitine-sensitive cdk that functions in neurons is cdk5, which is activated in part by its binding partner, p35. Because HSV establishes latent infections in sensory neurons, we sought to determine the role p35 plays in HSV-1 replication in vivo. For these studies, wild-type (wt) and p35−/− mice were infected with HSV-1 using the mouse ocular model of HSV latency and reactivation. The current results indicate that p35 is an important determinant of viral replication in vivo.
先前的研究表明，单纯疱疹病毒 1 型（HSV-1）的复制受到细胞周期蛋白依赖性激酶（cdk）抑制剂罗司维亭的抑制。在神经元中发挥作用的一种罗司维亭敏感的 cdk 是 cdk5，它部分通过其结合伴侣 p35 激活。由于 HSV 在感觉神经元中建立潜伏感染，我们试图确定 p35 在 HSV-1 在体内复制中的作用。在这些研究中，使用 HSV 潜伏和再激活的小鼠眼模型，用 HSV-1 感染野生型（wt）和 p35-/-小鼠。目前的结果表明，p35 是体内病毒复制的重要决定因素。
