武漢新冠病毒到底是否有可能是實驗室產物？

武漢病毒所石正麗及北卡大學實驗室主任Baric的名字在最後，按照生物醫學論文慣例，這個項目的老闆就是他們倆。

在石正麗，葛行義與北卡大學發表於2015年的《自然醫學》論文中，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設計與製作的，正是這位南亞學者及博士后，他是論文主要貢獻者，論文中該嵌合病毒的設計者及完成者，也正是他教會（壞）了武毒所的石正麗們。正像他所說的，"and what surprised us was that the SARS-like CoV spikes, WIV1 and SHC014, which were isolated from bats, caused robust disease."

（詳見其訪談錄，附錄在後）

另外，石正麗們10多年一直瘋狂捕捉蝙蝠分離冠狀病毒的經費從哪裡來？ 竟然是NIH 撥款，還有很大部分來自一個ECOHealth Alliance 的非盈利組織，而該組織也是美國政府撥款，部分來自捐款，比如比爾蓋茨等人。10多年前該組織有個設想，就是把全世界的病毒收集起來，分離並成立基因序列，建成病毒資料庫，因此獲得美國衛生部及NIH的大量撥款。

綜上，武漢新冠病毒的確與美國、法國、澳大利亞、加拿大等都有關係。

美國：支持武漢病毒所到處捕捉蝙蝠分離病毒，還教會石正麗們如何合成嵌合病毒感染人類；

法國：提供技術與設計圖紙幫助中共偽政權建造P4實驗室，石正麗、葛行義等人均在法國獲得博士學位並持續接受專業培訓。中共偽政權依據法國提供的P4實驗室圖紙自行建造的哈爾濱國家獸醫研究所P4實驗室，竟然在2013年對H1N1及H5N1病毒進行重組產生127種重配病毒，動物實驗發現三分之二以上對哺乳動物高度致死。並且合成病毒還獲得了自然演化沒有的功能提升-能通過空氣傳播；

澳洲： 石正麗們還在澳大利亞等實驗室開展各類深入的蝙蝠冠狀病毒及SARS病毒研究。

加拿大： 最近還和武漢病毒研究所一起就合作研究冠狀病毒事宜撥款。

也因此，這是一個龐大而完整的產業鏈及責任鏈，牽涉面太廣，這個蓋子能不能揭開的確是一個問題，也難怪你看到從NIH到法國、澳大利亞等等科學家都跳出來說這個病毒肯定不是實驗室合成，是自然產生的。不然，如果說是實驗室產生的，各種病毒實驗、細菌實驗、生物實驗被取締，想想多少人會飯碗不保？說不定還會有牢獄之災呢！     

所以，如果通過這次冠狀病毒瘟疫大爆發，美國等西方國家還不清醒，繼續開放大學，實驗室及國家衛生研究院（NIH)等科研院校與中共偽政權合作，為中共偽政權開放技術提供培訓，那將會繼續對全世界人類健康與生命造成巨大威脅！

希望通過這件事情，西方各國應該清醒了，是時候與中共偽政權全面脫鉤並開始追究責任了！

Emerging technologies to investigate coronavirus emergence – an interview with Vineet Menachery

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.