这里有一点关于演化的讨论 https://github.com/cov-lineages/pango-designation/issues/343 Many of these S mutations aren''t exactly common and quite a few are extremely rare. Aside from S371L which is unsurprisingly new since it is a 2nt mutation, all of N856K, Q954H, N969K, L981F have been seen fewer than 100 times. Q493K and Y505H were seen in the New York wastewater samples but are uncommon in humans (<200 samples). Lots more are rare enough that one wouldn''t suspect they were advantageous. It''s extremely unlikely that so many inconsequential mutations would accumulate in the spike rather than being more evenly spread through the genome, so the logical conclusion is that most of them are not inconsequential - even those ones from 856 to 981. Compare this with B.1.640 for example, where even the more odd-looking polymorphisms like N394S had been seen at least several hundred times before. (F490R was new but again that''s a 2nt mutation.) I''m not saying this is spillback from an animal reservoir after a year of adaptations in that species, but if that were to happen, this is the sort of thing it might look like. Edit: scratch that, the insertion is clearly human genome-derived. Unless that bit is shared with other mammals...? 值得思考 为啥这么多变异聚集在spike而不是散布在整个病毒的genome
这里有一点关于演化的讨论 https://github.com/cov-lineages/pango-designation/issues/343 Many of these S mutations aren''t exactly common and quite a few are extremely rare. Aside from S371L which is unsurprisingly new since it is a 2nt mutation, all of N856K, Q954H, N969K, L981F have been seen fewer than 100 times. Q493K and Y505H were seen in the New York wastewater samples but are uncommon in humans (<200 samples). Lots more are rare enough that one wouldn''t suspect they were advantageous. It''s extremely unlikely that so many inconsequential mutations would accumulate in the spike rather than being more evenly spread through the genome, so the logical conclusion is that most of them are not inconsequential - even those ones from 856 to 981. Compare this with B.1.640 for example, where even the more odd-looking polymorphisms like N394S had been seen at least several hundred times before. (F490R was new but again that''s a 2nt mutation.) I''m not saying this is spillback from an animal reservoir after a year of adaptations in that species, but if that were to happen, this is the sort of thing it might look like. Edit: scratch that, the insertion is clearly human genome-derived. Unless that bit is shared with other mammals...? 值得思考 为啥这么多变异聚集在spike而不是散布在整个病毒的genome
Hahaha 懂你要说的 well CleverBeaver 发表于 2021-11-25 23:55
不明白楼主没什么不提到，其实bloom认为antigenic selection might play substantial role. Trevor的那个chronic disease的解释不能解释为什么这么多的antigenic mutations. 也就是说，疫苗很有可能起了大的推动作用。是不是有fake news之嫌。 “selection on variants so far may be dominated more by transmissibility than antigenic selection (https://twitter.com/trvrb/status/1462816217794695170…). But I''m not as sanguine that antigenic selection isn''t also playing substantial role...“
不明白楼主没什么不提到，其实bloom认为antigenic selection might play substantial role. Trevor的那个chronic disease的解释不能解释为什么这么多的antigenic mutations. 也就是说，疫苗很有可能起了大的推动作用。是不是有fake news之嫌。 “selection on variants so far may be dominated more by transmissibility than antigenic selection (https://twitter.com/trvrb/status/1462816217794695170…). But I''m not as sanguine that antigenic selection isn''t also playing substantial role...“ Jxnc 发表于 2021-11-26 00:12
不明白楼主没什么不提到，其实bloom认为antigenic selection might play substantial role. Trevor的那个chronic disease的解释不能解释为什么这么多的antigenic mutations. 也就是说，疫苗很有可能起了大的推动作用。是不是有fake news之嫌。 “selection on variants so far may be dominated more by transmissibility than antigenic selection (https://twitter.com/trvrb/status/1462816217794695170…). But I''m not as sanguine that antigenic selection isn''t also playing substantial role...“ Jxnc 发表于 2021-11-26 00:12
这里有篇新出炉的文章 可以支持被lz忽略掉的antigenic selection的可能 搞不好nu的部分源头也和这有关 https://pubmed.ncbi.nlm.nih.gov/34314668/ Emergence of SARS-COV-2 Spike Protein Escape Mutation Q493R after Treatment for COVID-19 Daniele Focosi et al. Emerg Infect Dis. 2021 Oct. Abstract We report in vivo selection of a severe acute respiratory syndrome coronavirus 2 spike mutation (Q493R) conferring simultaneous resistance to bamlanivimab and etesivimab. This mutation was isolated from a patient who had coronavirus disease and was treated with these drugs. ————— Bamlanivimab is a monoclonal antibody developed by AbCellera Biologics and Eli Lilly as a treatment for COVID-19. The drug was granted an emergency use authorization by the US Food and Drug Administration in November 2020, and 950,000 doses have been bought by the US government as of December 2020. ————— 这个Q493R在香港病例里也出现了 https://m.posts.careerengine.us/p/619fa43038f1a94eff2e0fae
10号入住，11-14号overlap，20号才发现？ 我的妈，看起来潜伏期还挺长的。传染率高+潜伏期长+疫苗逃逸能力，感觉会是个王炸
我觉得未必是开门不戴口罩造成的 酒店通风系统，有15%新风就不错了，再利用的空气造成感染机率大多了
可以测序看突变，如果是同种不常见的突变，那被这个人传上的可能性很高。
流感疫苗从60年代开始打， 从上个世纪八十年开始普及， 到现在， 还没有人类灭绝丧尸来袭。
应该不管用了吧。 是不是需要新的疫苗？
疫苗重新做的话，是作为前面两，三针的一个booster， 还是要从第一针开始重新打，要再打至少两针呢？
美国不会ban的吧？
台上都是满口大爱的政客，感觉难。
这个。。。刚听说一例疑似booster诱发的autoimmune disease，不是年轻人都已过60了，现在上免疫球蛋白治疗了。。。
针对现有mrna疫苗的智能变异？
美国的官老爷们都休假了。英国速度真快，第一时间禁航南非。
这病毒真会挑时间。。。
听到中医就知道是个什么玩意了
每一次每一步节奏都踩得那么准，有没有?
先感染再疫苗的，我就知道川普一个。。。不知道先疫苗再感染再疫苗，有没有同等功效？
艾滋病人就是标准的免疫受损啊，动不动就各种病，免疫系统基本怠工，当然干不掉病毒了
英国禁航6个国家：南非、博茨瓦納、津巴布韋、納米比亞、萊索托和斯威士蘭。
Hahaha
懂你要说的
well
美国还是不禁
是的 潜伏巨长
嗯 没有selective pressure了
病毒自身也进化变聪明，病毒成功入侵宿主，首先是壳突蛋白结合宿主的受体的亲合力增强，自然是spike突变最多。
wow
这个。。。
所以病毒的速度永远比疫苗还快。
其实禁不禁的区别就是病毒早一点还是迟一点传播到美国。
如果大多数therapeutic efforts都集中在spike protein
。。。
对，口罩从出生戴到老死，物理隔离一万年。
不明白楼主没什么不提到，其实bloom认为antigenic selection might play substantial role. Trevor的那个chronic disease的解释不能解释为什么这么多的antigenic mutations. 也就是说，疫苗很有可能起了大的推动作用。是不是有fake news之嫌。
“selection on variants so far may be dominated more by transmissibility than antigenic selection (https://twitter.com/trvrb/status/1462816217794695170…). But I''m not as sanguine that antigenic selection isn''t also playing substantial role...“
或者免疫功能不好的病人治好以后多加观察 以防止超级变种的传播 这个可以有吧？
也有检测频率的影响，day 3, 5, 9检测。第二个病人是19号day 9检测，20号出结果。第一个病人是10或者11号飞机，13号 day 3 检测，14号出结果。
就是很快打了三针才算fully vaccinated. 当初疫苗设计是两针的剂量，中间间隔时间都有要求。现在加booster, trial走的完全把副作用消音了，难道这疫苗越打越安全，副作用越少？真神奇
就是中国，大大的赢家
就是同一个啊
两个居然都是breakthrough cases
但是至少测出来前他都无症状吧。 delta一般两三天就有症状了。
艾滋病啊
赢个毛，现在人员流动很受影响了，哪里有个无症状阳性，同区的人说黄码就黄码，说封小区就封，甚至去里面走个亲戚就有可能出不来了。很多人都不爱去外地打工了，经济不可能不受影响。
其实antigenic selection是很正常的思路 学过进化论的都知道
而且新冠不是还号称genome在RNA病毒里算很大的 就是因为它自带了一个纠错unit 所以之前大家都以为它变异速度极慢
谁知道就这样变种层出不穷了 还都是一个路数
不光是这样。s1 domain上有好多个mutations和transmissibility无关，但是和antigenic有关。你应该仔细看看，再下结论。
不打疫苗不让上飞机的
有一个病人已经有症状了。
欧美已经很多人都不戴口罩了。你戴但是感染的人不戴，基本没多大用。参见热门回复讨论的香港隔离的例子
我去， 这病毒载量很高啊。
在这个牛变种面前，副作用已经不值一提啦！第三针看起来对牛变种也没用了！
问：我可不可以不打第三针了？ 答：可以，你打第四针吧！🤣
我3月份打了强生，正在犹豫要不要跟风同事打booster。这个新变种出来，我就继续顶住公司压力暂时不打加强针。
N95还是有用的。
Xi 不用再变了 已经是领袖了
美国比加拿大多了7天，这是为啥？
多谢指点。看了一下nsp14 proof reading 的mechanism。虽然会减少mutation但是也提高了virus本身的存活率，这样应该会加快advantageous的mutations. 所以它的genome 虽然稳定，但是adoption可能还更快。
大部分国家都是14天，墨西哥也是。 美国曾经也是14天，甚至曾经缩短到7天，后来有一例隔离7天结束进入社区确诊的，引起了backfire，变成21天了。
建议没打疫苗的 趁着心理医生没有被挤兑之前赶紧去 免得心理精神悄悄出了问题报复社会
Hahaha
看到这图出处了 哎哎哎 life…
他和la jolla那位都是屁股坐哪儿脑袋就放哪儿了的典例吧
Ah icic
有道理的 fixation会更快！huaren上牛id真多
谢谢指教
那第二个病人15号做了 day 5检测，阴性。所以二号病人是11-14号之间感染，15号没事，19号阳性。潜伏期有可能比delta还是长一点？
可见做到客观公正太难了，总是会不自觉的偏向自己认定的观点，忽略对自己观点不利的因素
层主牛人！
这是活在自己相信的世界里。活得还挺认真。
我只是转述bloom的观点。过奖了。我也不是做病毒进化的。
这里有篇新出炉的文章 可以支持被lz忽略掉的antigenic selection的可能 搞不好nu的部分源头也和这有关
https://pubmed.ncbi.nlm.nih.gov/34314668/
Emergence of SARS-COV-2 Spike Protein Escape Mutation Q493R after Treatment for COVID-19 Daniele Focosi et al. Emerg Infect Dis. 2021 Oct.
Abstract We report in vivo selection of a severe acute respiratory syndrome coronavirus 2 spike mutation (Q493R) conferring simultaneous resistance to bamlanivimab and etesivimab. This mutation was isolated from a patient who had coronavirus disease and was treated with these drugs.
—————
Bamlanivimab is a monoclonal antibody developed by AbCellera Biologics and Eli Lilly as a treatment for COVID-19. The drug was granted an emergency use authorization by the US Food and Drug Administration in November 2020, and 950,000 doses have been bought by the US government as of December 2020.
—————
这个Q493R在香港病例里也出现了
https://m.posts.careerengine.us/p/619fa43038f1a94eff2e0fae
别人也没恐慌，就是打疫苗戴口罩不到处浪这三个办法，啥变种出来就这样吧，有啥好恐慌。
小孩就戴普通口罩就好了。前提是要人人戴，然后疫苗率高，就管用。
建议按期做基础体检，不要因为疫情推迟或者不做，怎么正常体检也成了疫苗铁杆的逆鳞了？疫苗多打几次强身健体不用体检了？
你管别人呢，你不愿意打疫苗就不打，还管别人去不去体检，管得真宽。
我是门外汉我不懂啊 大概看了下那个twitter thread 假设antigenic selection成立 那应对方法是啥？大家都不打疫苗吗？
这儿我感觉我有个observation bias啊 因为很多人打了疫苗 那变异出来的能breakthrough的引起大家注意的那不得就是那些在antigenic sites突破的吗。。而且这个的出现对没打疫苗的人也没差吧(vs一个非antigenic selection的变异）
不知道我理解的对不对啊 还望指正
但是楼主大谈是艾滋病人造成的变种，而不提到疫苗可能推动抗免疫，就有很大的误导之嫌。其实就是欺负大部分人不懂。
抗药性肯定会有，大面积使用是有可能造成selection pressure. 应该只给重症使用。
哈，对！健康体检千万别推迟，尤其是有家族史既往史需要按期随访的。两针mRNA打完出现免疫功能下降的不是一个两个，没数据证明，就是怀疑。不信的大可不信。所以有任何不适及时就医，别想着没什么事休息养养就能好，等症状明显了容易出问题。 打几针都没事的人，基因好，继续打呗，推广疫苗可能只需要你们的数据。
我觉得你去查查脑子，臆想症就是从絮絮叨叨开始的。
如果是真的，这个证明应该只给高危人群接种，大面积接种会推动危害整个人群的新变种，包括打了疫苗的。甚至针对打了疫苗的。
别人脑子好不好不知道，你的教养真的很差。