Immunocompromised 45 year old suffered from #COVID19 for 155 days before he died. The virus was changing very quickly inside the man's body—it acquired a big cluster of >20 mutations—resembled the same ones seen in #B117 & # B1351.
Dr. Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important."
Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron," Li says. "And shortly thereafter, we saw evidence that suggested the virus was developing resistance or escaping from these antibodies as well."
Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn — and this peculiar case in Boston took on a new importance.
Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries. When researchers looked at the genes of these variants, guess what they found?
A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren't exactly identical, but they shared important characteristics...
They both had about 20 mutations, and they shared several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and another mutation (E484K) known to help the virus evade antibody detection.
So we have a number of examples, around the planet, in which patients' viruses suddenly have a whole mess of new mutations all at once," says virologist Jeremy Luban at the University of Massachusetts Medical School. And other cases have likely gone undetected, he says.
So scientists are starting to think the two phenomena could be related. That perhaps new variants arose inside people similar to the man in Boston — that is, people who are immunocompromised & have long-term #COVID19 infections. "I think that's the leading theory," Luban says.
long-term infections are mutational testing ground. While inside 1 person, the virus can try out many different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious.
the moral lesson is that, when given time and opportunity, the virus finds a way. The virus is a cunning mutating beast that will try every way to defeat us if we let it keep proliferating. We must stop it FAST, or else it will even our countermeasures.
免疫功能低下的45岁老人在患上COVID-19 155天后死亡。该病毒在人体内的变化非常快。它获得了一个包含B117和B1351中所见的相似的20个突变的大簇。
李博士不敢相信他们的发现。他说：“我很震惊。” “当我看到病毒序列时，我知道
我们正在处理完全不同且可能非常重要的事物。”
李说：“在生命的尽头，他接受了来自再生元的单克隆抗体的治疗。此后不久，我们看到了证据表明该病毒也正在产生抗药性或从这些抗体中逃脱。”
李和他的同事们几乎没有大张旗鼓地将他们的发现发表在2020年11月的《新英格兰医学杂志》上。然后大约一个月后，大流行发生了令人惊讶的转变-波士顿的这一奇特案件
有了新的重要性。
英国和南非的科学家宣布，他们发现了冠状病毒的新变种。这些变体在这些国家引起了巨大的COVID-19激增。当研究人员查看这些变体的基因时，猜猜他们发现了什么？
看起来与波士顿病人的病毒中发现的突变非常相似的一组突变。突变的集合并不完全相同，但是它们具有重要的特征...
他们两个都有大约20个突变，并且共有几个关键突变，包括一个已知有助于病毒更紧密地与人细胞结合的突变（N501Y）和另一个有助于病毒逃避抗体检测的突变（E484K）。
因此，在地球上，我们有许多例子，其中患者的病毒突然之间突然都充满了新的突变。”马萨诸塞大学医学院的病毒学家杰里米·鲁班说。其他病例可能未被发现，他说。
因此，科学家开始认为这两种现象可能是相关的。与波士顿人相似的人内部可能出现了新的变异体，即免疫功能低下并长期感染＃COVID19的人。鲁班说：“我认为这是领先
的理论。”
长期感染是突变的试验场。在一个人内部时，该病毒可以尝试多种不同的突变组合，并通过反复试验找出最能逃避免疫系统或帮助病毒更具感染性的突变。
这个病例告诉我们，只要有时间和机会，病毒就会找到方法。该病毒是一种狡猾的变异野兽，如果我们让它继续繁殖，它将竭尽全力击败我们。我们必须尽快停止它，否则它将采取我们的对策。
Immunocompromised 45 year old suffered from #COVID19 for 155 days before he died. The virus was changing very quickly inside the man's body—it acquired a big cluster of >20 mutations—resembled the same ones seen in #B117 & #
B1351.
Dr. Li couldn't believe what they found. "I was shocked," he says. "When I
saw the virus sequences, I knew that we were dealing with something
completely different and potentially very important."
Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron," Li says. "And shortly thereafter, we saw evidence that
suggested the virus was developing resistance or escaping from these
antibodies as well."
Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month
later, the pandemic took a surprising turn — and this peculiar case in
Boston took on a new importance.
Scientists in the U.K. and South Africa announced they had detected new
variants of the coronavirus. These variants were causing huge surges of
COVID-19 in these countries.
When researchers looked at the genes of these variants, guess what they
found?
A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren't exactly identical, but they shared important characteristics...
They both had about 20 mutations, and they shared several key ones,
including a mutation (N501Y) known to help the virus bind more tightly to
human cells and another mutation (E484K) known to help the virus evade
antibody detection.
So we have a number of examples, around the planet, in which patients'
viruses suddenly have a whole mess of new mutations all at once," says
virologist Jeremy Luban at the University of Massachusetts Medical School.
And other cases have likely gone undetected, he says.
So scientists are starting to think the two phenomena could be related. That perhaps new variants arose inside people similar to the man in Boston —
that is, people who are immunocompromised & have long-term #COVID19
infections.
"I think that's the leading theory," Luban says.
long-term infections are mutational testing ground. While inside 1 person,
the virus can try out many different combinations of mutations and figure
out, through trial and error, which ones are best at evading the immune
system or helping the virus become more infectious.
the moral lesson is that, when given time and opportunity, the virus finds a way. The virus is a cunning mutating beast that will try every way to
defeat us if we let it keep proliferating. We must stop it FAST, or else it will even our countermeasures.
隔离封门 ~~ only way to go
强制隔离所有免疫力底下病人。
【 在 tran299 (熟道勇释放很少) 的大作中提到: 】
: 隔离封门 ~~ only way to go
45岁老人。。。
【 在 iminosugar (伪糖) 的大作中提到: 】
: 免疫功能低下的45岁老人在患上COVID-19 155天后死亡。该病毒在人体内的变化非常快
: 。它获得了一个包含B117和B1351中所见的相似的20个突变的大簇。
: 李博士不敢相信他们的发现。他说：“我很震惊。” “当我看到病毒序列时，我知道
: 我们正在处理完全不同且可能非常重要的事物。”
: 李说：“在生命的尽头，他接受了来自再生元的单克隆抗体的治疗。此后不久，我们看
: 到了证据表明该病毒也正在产生抗药性或从这些抗体中逃脱。”
: 李和他的同事们几乎没有大张旗鼓地将他们的发现发表在2020年11月的《新英格兰医学
: 杂志》上。然后大约一个月后，大流行发生了令人惊讶的转变-波士顿的这一奇特案件
: 有了新的重要性。
: 英国和南非的科学家宣布，他们发现了冠状病毒的新变种。这些变体在这些国家引起了
: ...................
说明就是人造的
【 在 iminosugar (伪糖) 的大作中提到: 】
: 免疫功能低下的45岁老人在患上COVID-19 155天后死亡。该病毒在人体内的变化非常快
: 。它获得了一个包含B117和B1351中所见的相似的20个突变的大簇。
: 李博士不敢相信他们的发现。他说：“我很震惊。” “当我看到病毒序列时，我知道
: 我们正在处理完全不同且可能非常重要的事物。”
: 李说：“在生命的尽头，他接受了来自再生元的单克隆抗体的治疗。此后不久，我们看
: 到了证据表明该病毒也正在产生抗药性或从这些抗体中逃脱。”
: 李和他的同事们几乎没有大张旗鼓地将他们的发现发表在2020年11月的《新英格兰医学
: 杂志》上。然后大约一个月后，大流行发生了令人惊讶的转变-波士顿的这一奇特案件
: 有了新的重要性。
: 英国和南非的科学家宣布，他们发现了冠状病毒的新变种。这些变体在这些国家引起了
: ...................