The Science Suggests a Wuhan Lab Leak The Covid-19 pathogen has a genetic footprint that has never been observed in a natural coronavirus. By Steven Quay and Richard Muller June 6, 2021 11:59 am ET 系统提示:若遇到视频无法播放请点击下方链接 https://www.youtube.com/embed/https://video-api.wsj.com/api-video/audio/iframe.html ILLUSTRATION: MARTIN KOZLOWSKI The possibility that the pandemic began with an escape from the Wuhan Institute of Virology is attracting fresh attention. President Biden has asked the national intelligence community to redouble efforts to investigate.[/iframe] But the most compelling reason to favor the lab leak hypothesis is firmly based in science. In particular, consider the genetic fingerprint of CoV-2, the novel coronavirus responsible for the disease Covid-19. In gain-of-function research, a microbiologist can increase the lethality of a coronavirus enormously by splicing a special sequence into its genome at a prime location. Doing this leaves no trace of manipulation. But it alters the virus spike protein, rendering it easier for the virus to inject genetic material into the victim cell. Since 1992 there have been at least 11 separate experiments adding a special sequence to the same location. The end result has always been supercharged viruses. A genome is a blueprint for the factory of a cell to make proteins. The language is made up of three-letter “words,” 64 in total, that represent the 20 different amino acids. For example, there are six different words for the amino acid arginine, the one that is often used in supercharging viruses. Every cell has a different preference for which word it likes to use most. In the case of the gain-of-function supercharge, other sequences could have been spliced into this same site. Instead of a CGG-CGG (known as “double CGG”) that tells the protein factory to make two arginine amino acids in a row, you’ll obtain equal lethality by splicing any one of 35 of the other two-word combinations for double arginine. If the insertion takes place naturally, say through recombination, then one of those 35 other sequences is far more likely to appear; CGG is rarely used in the class of coronaviruses that can recombine with CoV-2. In fact, in the entire class of coronaviruses that includes CoV-2, the CGG-CGG combination has never been found naturally. That means the common method of viruses picking up new skills, called recombination, cannot operate here. A virus simply cannot pick up a sequence from another virus if that sequence isn’t present in any other virus. Although the double CGG is suppressed naturally, the opposite is true in laboratory work. The insertion sequence of choice is the double CGG. That’s because it is readily available and convenient, and scientists have a great deal of experience inserting it. An additional advantage of the double CGG sequence compared with the other 35 possible choices: It creates a useful beacon that permits the scientists to track the insertion in the laboratory. Now the damning fact. It was this exact sequence that appears in CoV-2. Proponents of zoonotic origin must explain why the novel coronavirus, when it mutated or recombined, happened to pick its least favorite combination, the double CGG. Why did it replicate the choice the lab’s gain-of-function researchers would have made? Yes, it could have happened randomly, through mutations. But do you believe that? At the minimum, this fact—that the coronavirus, with all its random possibilities, took the rare and unnatural combination used by human researchers—implies that the leading theory for the origin of the coronavirus must be laboratory escape. When the lab’s Shi Zhengli and colleagues published a paper in February 2020 with the virus’s partial genome, they omitted any mention of the special sequence that supercharges the virus or the rare double CGG section. Yet the fingerprint is easily identified in the data that accompanied the paper. Was it omitted in the hope that nobody would notice this evidence of the gain-of-function origin? But in a matter of weeks virologists Bruno Coutard and colleagues their discovery of the sequence in CoV-2 and its novel supercharged site. Double CGG is there; you only have to look. They comment in their paper that the protein that held it “may provide a gain-of-function” capability to the virus, “for efficient spreading” to humans. There is additional scientific evidence that points to CoV-2’s gain-of-function origin. The most compelling is the dramatic differences in the genetic diversity of CoV-2, compared with the coronaviruses responsible for SARS and MERS. Both of those were confirmed to have a natural origin; the viruses evolved rapidly as they spread through the human population, until the most contagious forms dominated. Covid-19 didn’t work that way. It appeared in humans already adapted into an extremely contagious version. No serious viral “improvement” took place until a minor variation occurred many months later in England. Such early optimization is unprecedented, and it suggests a long period of adaptation that predated its public spread. Science knows of only one way that could be achieved: simulated natural evolution, growing the virus on human cells until the optimum is achieved. That is precisely what is done in gain-of-function research. Mice that are genetically modified to have the same coronavirus receptor as humans, called “humanized mice,” are repeatedly exposed to the virus to encourage adaptation. The presence of the double CGG sequence is strong evidence of gene splicing, and the absence of diversity in the public outbreak suggests gain-of-function acceleration. The scientific evidence points to the conclusion that the virus was developed in a laboratory. Dr. Quay is founder of Atossa Therapeutics and author of “Stay Safe: A Physician’s Guide to Survive Coronavirus.” Mr. Muller is an emeritus professor of physics at the University of California Berkeley and a former senior scientist at the Lawrence Berkeley National Laboratory.
那位大牛以前开过physics for future presidents的课 所以写起科普文来游刃有余
我也没有权限 早上用的免费权限看的 其实就是拎了一下重点 没有新内容 thumbnail picture用的也是旧的
评论区涨的飞快 有人呼吁可以炒掉Fauci了
DRASTIC那帮人又开始盯Anderson同学的旧推怎么都删掉了 A同学自称是cronjob auto delete的 D帮在找人工删除的痕迹 有点搞。。。
edit: apple news里找到了 上渣图
这篇文章主要说的就是从科学角度来看,最合理的解释就是这个病毒是在实验室通过功能增益搞出来的。主要两个证据:
1。基因序列里有CGG-CGG,这种组合在自然界很罕见而在实验室却是最常用的方法。石正丽发表新冠基因序列的时候对这种罕见的情况绝口不提让人生疑。支持自然起源的人需要解释为什么一个病毒会选择自然界最不可能而人类实验室最常用的方法?
2。自然演化的病毒包括SARS和MERS都有一个共性,就是它们经过了很多变异才会形成对人有高传染性。但是这次的COV-2却不一样,它是一上来就已经是极其适合在人群中传播了。这个非常符合功能增益的特点。实验室里要做到这一点一般是先搞出拥有类似人类器官的小白鼠,通过他们的器官来完成变异过程。这样一出来就适应人类。
我自己加一句:中国被爆出在2019年9月就已经在具有人肺的小白鼠身上做实验了。
多谢转发,这个cgg-cgg有没懂的人?这要坐实了,大概大家要30年不能回国了。
感谢mm的拎重点!
为什么? 中国一小撮人犯罪等于全部华人都犯罪?
其他华人跟着倒霉 背锅
你social security 搞清楚了?
系统提示:若遇到视频无法播放请点击下方链接
https://www.youtube.com/embed/https://video-api.wsj.com/api-video/audio/iframe.html ILLUSTRATION: MARTIN KOZLOWSKI The possibility that the pandemic began with an escape from the Wuhan Institute of Virology is attracting fresh attention. President Biden has asked the national intelligence community to redouble efforts to investigate.[/iframe]
But the most compelling reason to favor the lab leak hypothesis is firmly based in science. In particular, consider the genetic fingerprint of CoV-2, the novel coronavirus responsible for the disease Covid-19. In gain-of-function research, a microbiologist can increase the lethality of a coronavirus enormously by splicing a special sequence into its genome at a prime location. Doing this leaves no trace of manipulation. But it alters the virus spike protein, rendering it easier for the virus to inject genetic material into the victim cell. Since 1992 there have been at least 11 separate experiments adding a special sequence to the same location. The end result has always been supercharged viruses. A genome is a blueprint for the factory of a cell to make proteins. The language is made up of three-letter “words,” 64 in total, that represent the 20 different amino acids. For example, there are six different words for the amino acid arginine, the one that is often used in supercharging viruses. Every cell has a different preference for which word it likes to use most. In the case of the gain-of-function supercharge, other sequences could have been spliced into this same site. Instead of a CGG-CGG (known as “double CGG”) that tells the protein factory to make two arginine amino acids in a row, you’ll obtain equal lethality by splicing any one of 35 of the other two-word combinations for double arginine. If the insertion takes place naturally, say through recombination, then one of those 35 other sequences is far more likely to appear; CGG is rarely used in the class of coronaviruses that can recombine with CoV-2. In fact, in the entire class of coronaviruses that includes CoV-2, the CGG-CGG combination has never been found naturally. That means the common method of viruses picking up new skills, called recombination, cannot operate here. A virus simply cannot pick up a sequence from another virus if that sequence isn’t present in any other virus. Although the double CGG is suppressed naturally, the opposite is true in laboratory work. The insertion sequence of choice is the double CGG. That’s because it is readily available and convenient, and scientists have a great deal of experience inserting it. An additional advantage of the double CGG sequence compared with the other 35 possible choices: It creates a useful beacon that permits the scientists to track the insertion in the laboratory. Now the damning fact. It was this exact sequence that appears in CoV-2. Proponents of zoonotic origin must explain why the novel coronavirus, when it mutated or recombined, happened to pick its least favorite combination, the double CGG. Why did it replicate the choice the lab’s gain-of-function researchers would have made? Yes, it could have happened randomly, through mutations. But do you believe that? At the minimum, this fact—that the coronavirus, with all its random possibilities, took the rare and unnatural combination used by human researchers—implies that the leading theory for the origin of the coronavirus must be laboratory escape. When the lab’s Shi Zhengli and colleagues published a paper in February 2020 with the virus’s partial genome, they omitted any mention of the special sequence that supercharges the virus or the rare double CGG section. Yet the fingerprint is easily identified in the data that accompanied the paper. Was it omitted in the hope that nobody would notice this evidence of the gain-of-function origin? But in a matter of weeks virologists Bruno Coutard and colleagues their discovery of the sequence in CoV-2 and its novel supercharged site. Double CGG is there; you only have to look. They comment in their paper that the protein that held it “may provide a gain-of-function” capability to the virus, “for efficient spreading” to humans. There is additional scientific evidence that points to CoV-2’s gain-of-function origin. The most compelling is the dramatic differences in the genetic diversity of CoV-2, compared with the coronaviruses responsible for SARS and MERS. Both of those were confirmed to have a natural origin; the viruses evolved rapidly as they spread through the human population, until the most contagious forms dominated. Covid-19 didn’t work that way. It appeared in humans already adapted into an extremely contagious version. No serious viral “improvement” took place until a minor variation occurred many months later in England. Such early optimization is unprecedented, and it suggests a long period of adaptation that predated its public spread. Science knows of only one way that could be achieved: simulated natural evolution, growing the virus on human cells until the optimum is achieved. That is precisely what is done in gain-of-function research. Mice that are genetically modified to have the same coronavirus receptor as humans, called “humanized mice,” are repeatedly exposed to the virus to encourage adaptation. The presence of the double CGG sequence is strong evidence of gene splicing, and the absence of diversity in the public outbreak suggests gain-of-function acceleration. The scientific evidence points to the conclusion that the virus was developed in a laboratory. Dr. Quay is founder of Atossa Therapeutics and author of “Stay Safe: A Physician’s Guide to Survive Coronavirus.” Mr. Muller is an emeritus professor of physics at the University of California Berkeley and a former senior scientist at the Lawrence Berkeley National Laboratory.
应该先问问FB Fauci 这些“科学权威” 当时是怎么“fact check”的 现在改口了?
美国人真是蠢 死了六十万都不知道是怎么死的 那些电影里为家人报仇的英雄呢?
中国只有闭关锁国了,说西方联合冤枉它。
不要曲解他们的话,他们没说这个证明了lab leak,而是说从目前信息看起来这是最合理的解释。
是的
这里又有个新闻采访视频 有人实名认证 说Fauci去年年初就告诉欧洲各国领导人很可能是lab leak
https://twitter.com/facethenation/status/1401566810265247747?s=21
系统提示:若遇到视频无法播放请点击下方链接
https://twitter.com/i/videos/1401566810265247747
要证明一件事不能用另外一件不太可能的事去证明其他事情。这个是非常基本的道理,去年大家都有integrity,今年有些人就开始耍无赖了。
五毛继续洗地
美国没有证据就诬赖别人的事情还不够多吗?伊拉克杀伤武器,中国芯片里能骇客信息,中国4G会窃听消息,等等。现在有说新冠是实验室造的,有确切证据说没问题,没有证据bb只能显示无能。
谢谢顶帖
Andersen同学彻底退出推特了
等瓜
其实中国印度都有特殊的环境,光一个过敏,哮喘,就够医学界喝一壶的,但是中印出生的很多人对鸡蛋和花生不过敏。
我觉得,中国的生鲜市场,地沟油,滥用抗生素,是培养超级病毒的绝佳场所
Kristian G. Andersen不但退出了推特,连LinkedIn profile也删得干干净净。
但是他自己在Scripps的官网主页上的Twitter和LinkedIn的链接都还没来得及改。
是的,这些都不是direct evidence而是circumstantial evidence,但判案只要circumstantial evidence足够强也是可以定罪的。就像保安发现今天所有进楼的人都提着湿漉漉的伞或者淋成落汤鸡,那么即使他看不到外面的天,也可以断定外面下雨的,虽然也存在所有今天进楼的人都是为了逗保安玩这个可能。
现在说是因为让说了,前几天facebook还不让说这事呢,谁说谁是反动的阴谋论患者
有一个比较重要的转折是大家发现去年二月发表在柳叶刀上的24名专家联署信的幕后推手其实是Peter Daszak,虽然他们宣称参与者不涉利益冲突,大大降低了那份声明的公信力。
抓住一只五毛
睿大妈都被抓无数次了,当成反指就行了,而且绝对稳定可靠,现在大新闻没她出来反指确认都不敢信。
谢谢提醒 这家伙很助纣为虐呀 压制言论自由的措辞daszak还得听他的
跑去搜了一个他去年四月的视频 根本不提为啥lab origin是不可能的 只说了一句 our data says so
感觉骗了我们或对我们隐瞒了真相 还是为我们好
刚看到,好像本版已经贴过了?
我个人认为已有足够circumstantial evidence是。 其实就像犯罪,很少嫌犯是现行犯罪(crime in action) 被抓的,所以,只要 是beyond reasonable doubt 就可以定罪。
想看团伙成员都怎样跳船
本主题没有人这样说,所以要有的放矢。如果我没有弄错,你的高论“只有从欧美才能查个水落石出”,何时可以发挥一下。
你这样责怪受害者们,不太道德。
对的,今年WHO被中国政府劫持发表的洗地报告使科学界震动不已。中国政府玩此地无银三百两到了极致,现在被反弹也是重要原因之一。
我在隔壁楼说了去年初得新冠了 其实说过n遍了 但隔壁那楼十分诡异 属于只能说好不能说不好的 于是我先被说不打疫苗就是破罐破摔 再被说得过新冠就会有严重后遗症
有时候难免觉得新冠的出现也真不是个坏事
人心真的不能直视
罪与错还是本质不同。
为了funding误导民众 造成大量死亡 好像的确不犯法
舆论准备需要个过程,慢慢发酵。其他准备应该提前就绪了。
手动赞
其实不用这么麻烦,以前因为一包洗衣粉都能把别的国家炸个稀巴烂,只要美国认为,就可以了,直接动武就行。
那是伊拉克没有核武器,各方面实力都无法和中国相提并论。能比吗?
你没测试怎么知道得的是新冠?很大可能根本不是。
川粉不是说:川皇输掉,最合理的解释是大选舞弊吗? 现代社会,什么时候最合理的解释可以作为证据?这不是阴谋论的标准定义么
装睡的人永远叫不醒。。。
把当年的“一包洗衣粉” 跟现在能找到的这么多 circumstantial evidence类比,也算是服了你了
太健忘了,当年的"circumstantial evidence"可比现在多多了
可以举几个例子吗?
陪审团干什么用的?在没有绝对证据的时候,就是靠陪审团来决定证据是否足以判决有罪。在这里也是一样,只要大家都认为证据足够,就够了。
“我自己加一句:中国被爆出在2019年9月就已经在具有人肺的小白鼠身上做实验了。” 来源请提供。
科学的结论是通过统计得出的, 统计表明基因序列CGG-CGG,这种组合在自然界出现的可能性小到可以忽略的地步,而实验室出现的可能性几乎是100%,这就是很充分的科学证据。至于那个昭著的ID “睿” 拿政治说事,与科学风马牛不相及。
他们玩这一套又不是一天俩天。其实这样咋胡咋胡的,中国墙内人搞不到,搞的都是华人。
President Biden: "Yes, I'm very confident in Dr. Fauci."
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https://twitter.com/i/videos/1400828350684336132
看来你是非常积极的自然发生论者,或投毒论者。今天愿意听一下你的科学论据如何?