Nature Commun:是什么让禽流感跨越物种屏障
2017/04/03
是什么让禽流感病毒突破种属的屏障?科学家终于有了答案,就在区区一个单碱基上。香港大学的研究人员发表在Nature Communication上的一篇论文报道了相关内容。


香港大学的研究人员3月21日发表在Nature Communication上的一篇论文报道了H7N9禽流感病毒RNA序列的一个碱基的改变可以解释其持续感染人类和鸟类的能力。

禽流感,全名鸟禽类流行性感冒,是由病毒引发的动物传染病,通常只感染鸟类,少见情况会感染猪,在罕有情况下会跨越物种障碍感染人。2013年初以来,H7N9已经导致超过1000人患病,约有40%的病例被证实是致命的。

是什么让禽流感“步步升级”?是什么让禽流感病毒突破种属的屏障?科学家终于有了答案,就在区区一个单碱基上(如下图)。


NS mRNA拼接的整体调节机制

参考资料

An NS-segment exonic splicing enhancer regulates influenza A virus replication in mammalian cells

What makes bird flu jump species?

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  • An NS-segment exonic splicing enhancer regulates influenza A virus replication in mammalian cells

    Influenza virus utilizes host splicing machinery to process viral mRNAs expressed from both M and NS segments. Through genetic analysis and functional characterization, we here show that the NS segment of H7N9 virus contains a unique G540A substitution, located within a previously undefined exonic splicing enhancer (ESE) motif present in the NEP mRNA of influenza A viruses. G540A supports virus replication in mammalian cells while retaining replication ability in avian cells. Host splicing regulator, SF2, interacts with this ESE to regulate splicing of NEP/NS1 mRNA and G540A substitution affects SF2–ESE interaction. The NS1 protein directly interacts with SF2 in the nucleus and modulates splicing of NS mRNAs during virus replication. We demonstrate that splicing of NEP/NS1 mRNA is regulated through a cis NEP-ESE motif and suggest a unique NEP-ESE may contribute to provide H7N9 virus with the ability to both circulate efficiently in avian hosts and replicate in mammalian cells.

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