首先我们回顾一下SUMMARY：
Knockdown or knockout of USP38 increases K48-linked ubiquitination and degradation of TBK1,thus enhancing type I IFN signing.
从题目可以看出，本部分是对SMMARY这一部分的阐明。
并且，在Result1中得出的结论：
……suggesting that USP38 inhibits the expression of IFN-stimulated genes(ISGs)…Collectively,these results suggest that USP38 negatively regulates type I IFN signing as well as antiviral immunity human cell types.
那么，作为条件对照，说明USP38 缺失对抗病毒免疫的作用是必要的.
尽管Results1中有：
Further we showed that USP38 knockdown in this cells rendered them resistant to VSV-EGFP infection.
但由于都是体外实验，所以这里进行体内实验.
于是，实验一，利用人工培育的USP38缺陷的小鼠进行细胞水平验证.
To determine the fuction of USP38 in primary cells,we generated USP38-deficient mice using a TAL effector nuclease (TALEN)-based system,and we prepared bone marrow-derived macrophages(BMMs) from wild-type(WT) and Usp38`/` mice.Next we infected those BMMs for 16 or 24 hr with the RNA virus VSV or the DNA virus HSV-1.
结果是：
USP38ˉ/ ˉBMMs produce 2- to 4-fold more IFN-阝in responds to VSV or HSV-1 than WT BMMs.
…deletion of USP38 had a strong effect on the expression of many ISGs…as well as the pro-inflammatory cytokines TNF-∝and IL-6……
We detected significantly less VSV or HSV-1 in USP38ˉ/ˉ BMMs than in WT BMMs.These data indicate a negative role for USP38 in the sensing of both RNA and DNA viruses in mouse BMMs.
接着是实验二，在器官个体水平的实验，不过这次为了更好说明USP38的"functional significance",使用了高浓度病毒VSV.结果是：
器官水平：
……We found that VSV loads in tissue sample infected Usp38'/' mice were significantly lower than those from WT mice 24 hr post-infection.
个体水平：
Importantly,Usp38ˉ/ˉ mice were signifcantly more resistant to VSV infection in overall survival compared with WT mice.
于是自然得出结论：USP38 Deficiency Enhances Antiviral Immunity In Vivo
陌生概念：
plaque-forming units(PFU)：空斑形成单位，是一种测量每单位体积可以形成斑块的颗粒数量的办法；是一种功能性的测量，有缺陷或不影响目标细胞的病毒颗粒不产生斑块.
最后是思考题：
