rojjer 发表于 2016-5-25 23:53
这篇文章我觉得是研究之前就知道结果了吧，按照套路把改补的实验补了，创新只能说是zika.
赶紧反向遗传，删 ...

zika NS5具有抑制IFN功能推测出有,但是机制不一样，又没有做出来，要不是zika这么火，这文章最多发virology

这篇文章我觉得是研究之前就知道结果了吧，按照套路把改补的实验补了，创新只能说是zika.
赶紧反向遗传，删除Ns5关键位点做个减毒活疫苗。

E3酶也还没找到呢，再找下为什么不能跟鼠STAT2结合，这篇文章应该继续做了发个大文章。估计是也有人在做，估计是抢发吧。

Zika Virus Targets Human STAT2 to Inhibit Type I Interferon Signaling

Alesha Grant, Sanket S. Ponia, Shashank Tripathi, Vinod Balasubramaniam, Lisa Miorin, Marion Sourisseau, Megan C. Schwarz, Mari Paz Sánchez-Seco, Matthew J. Evans, Sonja M. Best, Adolfo García-Sastre

Highlights
•Flavivirus nonstructural NS5 proteins antagonize type I IFN by different mechanisms
•Zika virus (ZIKV) NS5 targets the IFN-regulated transcriptional activator STAT2
•ZIKV NS5 binds to and targets human, but not mouse, STAT2 for degradation
•Unlike dengue, ZIKV NS5-mediated STAT2 degradation does not require E3 ligase UBR4

Summary
The ongoing epidemic of Zika virus (ZIKV) illustrates the importance of flaviviruses as emerging human pathogens. All vector-borne flaviviruses studied thus far have to overcome type I interferon (IFN) to replicate and cause disease in vertebrates. The mechanism(s) by which ZIKV antagonizes IFN signaling is unknown. Here, we report that the nonstructural protein NS5 of ZIKV and other flaviviruses examined could suppress IFN signaling, but through different mechanisms. ZIKV NS5 expression resulted in proteasomal degradation of the IFN-regulated transcriptional activator STAT2 from humans, but not mice, which may explain the requirement for IFN deficiency to observe ZIKV-induced disease in mice. The mechanism of ZIKV NS5 resembles dengue virus (DENV) NS5 and not its closer relative, Spondweni virus (SPOV). However, unlike DENV, ZIKV did not require the E3 ubiquitin ligase UBR4 to induce STAT2 degradation. Hence, flavivirus NS5 proteins exhibit a remarkable functional convergence in IFN antagonism, albeit by virus-specific mechanisms.

http://www.cell.com/cell-host-microbe/abstract/S1931-3128(16)30205-0