這個是我在疫情爆發後不久寫的。
寫於2020年4月
沒有依據，那請拿出新冠病毒不是起源於實驗室的依據啊？ 另外，如何解釋2015年石正麗與北卡大學一起用小白鼠定植的SARS病毒做骨架，加入冠狀病毒形成新的嵌合病毒並引發直接感染人體細胞並無藥可救的論文，以及今年2月22日瑞士科研團隊發表論文，在沒有新冠病毒實體而僅僅依靠已知新冠病毒基因序列的基礎上，通過反向遺傳學手段在酵母菌中快速構建出了活的新冠病毒，可在一周內產出大量病毒活體。https://new.qq.com/omn/20200225/20200225A0BGEJ00.html
下麵這個鏈接，是對該論文主要作者（生化論文慣例：排名第一就是主要貢獻者，最後是老板） 原北卡大學博士後，現德州大學副教授 VINEET MENACHERY的采訪。可惜在對實驗室泄漏論提出後，被刪除了。
不過我節錄部分還在，可以一窺其究竟。
Recent decades have seen the emergence of several zoonotic coronaviruses (CoV), from the first outbreak of SARS to the ongoing cases of MERS in the Middle East. However, with major advances in fields such as genomics and structural biology, can more be uncovered about coronaviruses and their emergence?
In this interview we speak to Vineet Menachery about his recent talk at the Microbiology Society’s Annual Conference (8–11 April, Belfast, UK) suggesting that coronavirus emergence is more complicated than receptor binding alone.
First, could you introduce yourself and give a brief summary your career to date?
I started as a PhD student at Washington University in Saint Louis (MO, USA). I was in the immunology program, but always interested in virology. I did my PhD with David Leib (Geisel School of Medicine at Dartmouth, NH, USA), who was a herpes virologist, and then from David’s lab, I went to Ralph Baric’s lab at the University of North Carolina (NC, USA) in 2010 to study coronaviruses.
So, I had been interested in type one interferon and interferon-stimulated genes and that is what I worked on initially when I was at Ralph’s lab. Then the opportunity came up to work with bat CoVs, which was obviously a great opportunity. My lab also works on the host side looking at aging in the context of SARS and MERS infections and we have funding from the NIH to work on that, in addition to our research on bat viruses.
Could you outline the research you’re presenting here?
So, in my talk I talked about a longitudinal study that had been done by Zhengli Shi’s group at the Wuhan Institute [1] on Chinese horseshoe bats, which led to a big shift in our thinking about these bat CoVs because it revealed they are much closer to the epidemic SARS strains than previously thought. Normally, we don’t evaluate anything beyond being reactive to the next emergent strain, but building on this study using our infectious clone system we had the opportunity to ask more questions – and that’s how this project started.
“Normally, we don’t evaluate anything beyond being reactive to the next emergent strain, but building on this study using our infectious clone system we had the opportunity to ask more questions – and that’s how this project started.”The study that I showed was using a chimeric approach – taking the spike protein of bat CoVs and putting them into the backbone of a virus we knew was functional. Coronaviruses are really large, so with generating the viruses there are any number of other things that could go wrong, such as incompatibilities, that might not allow that virus replicate even though the spike might be viable – by putting just the spike in a known backbone we could gain some insight into that. We chose a mouse-adapted strain for the backbone because then we could take the chimeric virus into animals, and what surprised us was that the SARS-like CoV spikes, WIV1 and SHC014, which were isolated from bats, caused robust disease.
我展示的研究使用的是嵌合方法-提取蝙蝠冠狀病毒的刺突蛋白，並將其放入我們已知具有功能的病毒的骨架中。
德州大學副教授 VINEET MENACHERY:
