”This is about Saving Lives”「命を救うぞ！」と「Protein 14」をちょちょいといじくったら「14へ行け」が出ますた！（爆ｗ

 

Infidelity of SARS-CoV Nsp14-Exonuclease Mutant Virus Replication Is Revealed by Complete Genome Sequencing

• Lance D. Eckerle,
• Michelle M. Becker,
• Rebecca A. Halpin,
• Kelvin Li,
• Eli Venter,
• Xiaotao Lu,
• Sana Scherbakova,
• Rachel L. Graham,
• Ralph S. Baric,
• Timothy B. Stockwell,
• David J. Spiro,
• Mark R. Denison

• Published: May 6, 2010
• https://doi.org/10.1371/journal.ppat.1000896

Abstract

Most RNA viruses lack the mechanisms to recognize and correct mutations that arise during genome replication, resulting in quasispecies diversity that is required for pathogenesis and adaptation. However, it is not known how viruses encoding large viral RNA genomes such as the Coronaviridae (26 to 32 kb) balance the requirements for genome stability and quasispecies diversity. Further, the limits of replication infidelity during replication of large RNA genomes and how decreased fidelity impacts virus fitness over time are not known. Our previous work demonstrated that genetic inactivation of the coronavirus exoribonuclease (ExoN) in nonstructural protein 14 (nsp14) of murine hepatitis virus results in a 15-fold decrease in replication fidelity. However, it is not known whether nsp14-ExoN is required for replication fidelity of all coronaviruses, nor the impact of decreased fidelity on genome diversity and fitness during replication and passage. We report here the engineering and recovery of nsp14-ExoN mutant viruses of severe acute respiratory syndrome coronavirus (SARS-CoV) that have stable growth defects and demonstrate a 21-fold increase in mutation frequency during replication in culture. Analysis of complete genome sequences from SARS-ExoN mutant viral clones revealed unique mutation sets in every genome examined from the same round of replication and a total of 100 unique mutations across the genome. Using novel bioinformatic tools and deep sequencing across the full-length genome following 10 population passages in vitro, we demonstrate retention of ExoN mutations and continued increased diversity and mutational load compared to wild-type SARS-CoV. The results define a novel genetic and bioinformatics model for introduction and identification of multi-allelic mutations in replication competent viruses that will be powerful tools for testing the effects of decreased fidelity and increased quasispecies diversity on viral replication, pathogenesis, and evolution.

Funding: This work was supported by Public Health Service awards from the National Institute of Allergy and Infectious Diseases T32-AI049824 (LDE); R01-AI026603 (MRD); P01-AI059443 (RSB and RLG); F32-AI080148 (RLG); U54-AI057157 (MMB); and NIH contract N01-AI-30071 and HHSN272200900007C (DJS). Additional support was provided by Public Health Service award CA68485 to the Vanderbilt University DNA Sequencing Shared Resource of the Vanderbilt-Ingram Cancer Center. The funding organizations had no role in study design, data collection or analysis, or preparation of the manuscript.

https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1000896

コロナウイルス (SARS-CoV)の変異のスピードが２１倍にアップしたとさ・・・（爆ｗｗｗｗｗｗｗｗｗｗ

で、まあワクチンもあるし大丈夫だと８２もちょちょいいじくってみたら・・・ 

2022年3月26日土曜日

ピザを食らうBiden@82 Airborne
https://tokumei10.blogspot.com/2022/03/biden82-airborne.html

2022年3月26日土曜日

流出したのがキメラ肺ペストだけだとは限らない件

 The responsible strain, named Makona, carries an A-to-V substitution at position 82 (A82V) in the glycoprotein (GP), which is associated with enhanced infectivity in vitro. 

An effective experimental vaccine for Ebola exists, and more than a hundred and seventy-five thousand people have received it. Even so, the virus is finding new victims and extending its geographic range. Three cases of Ebola recently appeared in Uganda, and there have now been four cases in the Congolese city of Goma, which has roughly two million residents and is situated on the border with Rwanda. The W.H.O. recently estimated that more than two hundred million dollars in emergency funding would be needed to bring the virus under control. That money hasn’t been raised yet.

Ebola particles copy themselves every eighteen hours. This is the generation time of the virus—the time it takes for a particle of Ebola to get inside a human cell and potentially create thousands of identical copies of itself in the cell.

 Some virologists wonder whether Kivu Ebola could start evolving, or whether it has already started to evolve, in a way that makes it more dangerous to people—perhaps by becoming more contagious, in which case it would get much harder to control. These questions introduce a new aspect to the international emergency.

During the Ebola epidemic that ravaged West Africa in 2014 and 2015, that form of Ebola showed possible signs of evolving. Virologists are still trying to determine the significance of what happened. The epidemic began in a village in Guinea, in December, 2013, when some particles of Ebola apparently went from a bat into a small boy. That strain of the virus, now referred to as Makona Ebola, killed the boy and most of his family, and then began spreading. In the end, around thirty thousand people were infected and more than eleven thousand died before Makona Ebola was finally brought under control and eliminated from the human population. (There were eleven cases in the United States.)

As the epidemic progressed, a team of researchers, led by Pardis Sabeti, a genomic scientist at Harvard and the Broad Institute, studied the genetic code of various samples of Ebola taken from the blood of people who had been infected. They found that the virus began mutating as soon as it got into people. “From the outset, I was intrigued by the large number of mutations we found,” Sabeti told me. Makona Ebola quickly developed into several basic varieties. Then, in late May, 2014, one of the lineages took off like a wildfire and spread rapidly all over Sierra Leone and Liberia. This lineage is named the A82V Makona Variant of Ebola. For simplicity, I’ll call it the Makona mutant. The majority of patients in the epidemic were infected with the Makona mutant, including all eleven individuals in the United States. Meanwhile, the other lineages of Ebola died out. It seemed that the Makona mutant had somehow beaten them in a contest for survival.

https://tokumei10.blogspot.com/2022/03/blog-post_98.html

18時間毎に変異し、免疫力をアップさせるワクチンじゃ全然感染拡大を防げなくなるだけじゃなく病原体の戦闘力と防御力と変異の速度をレベルアップさせる結果を招くだけの使っちゃいけない対策になってしまいました。(๑´ڡ`๑)てへぺロ♡

2022年3月23日水曜日

武漢で本当は何が起きたのか？

映画とかでよくあるウイルス＋ワクチン＝完成したバイオ兵器というすり込みにより多くの人が勘違いしてるが、ウイルス＋ワクチンによる完全なバイオ兵器ってのは不可能。

・・・ってかそもそもワクチンはその危険なバイオ兵器をさらに制御不能なヤバイもんに変異させる可能性があるので最初からアウト！（爆ｗｗｗｗｗ

それならどうすれば良いか。

https://tokumei10.blogspot.com/2022/03/blog-post_51.html

だから・・・

2022年3月24日木曜日

高学歴の研究者なんて皆、例外なく勉強という名の脳の筋トレばっかやりまくった真の「脳筋」だと知らない低学歴のDQNや引き籠りやキモオタ以下のウンコ

https://tokumei10.blogspot.com/2022/03/dqn.html

・・・と。（爆ｗｗｗｗｗｗｗｗｗｗｗｗｗｗｗｗｗｗｗ

2021年12月19日日曜日

14へ行け じゅうよんへいけ 14平家

14へ行け

じゅうよんへいけ

             「14へ行け」とは一種の死亡宣告である。

J・H・ブレナン作のゲームブック「グレイルクエスト」（旧「ドラゴン・ファンタジー」）シリーズではプレイヤーキャラクターであるピップが死亡した場合に誘導されるパラグラフ番号が14に固定されている。
戦闘で生命点が尽きたら「14へ行け」、致死性のトラップにかかると「14へ行け」、詩的魔神（※）の機嫌を損ねても「14へ行け」…とにかく「14へ行け」なのである。

そこからこの作品を知っている人間の間では「14へ行け」と言う言葉は、相手がもう死に体である事を教えてやりたい時や、「死ね」と罵ってやりたい時等に代わりに使われることがある。

※ 同シリーズの名物キャラクター。一応は友好的な存在だが、彼の詩をけなすなどして怒らせてしまうと殺されてしまう。ちなみにその際、他の怪物等が相手の時と違って戦闘にはならず、何の抵抗も出来ずあっという間に14行きとなる。 

dic.pixiv.net/a/14へ行け

https://tokumei10.blogspot.com/2021/12/14-14.html

2022年3月20日日曜日

「命を救うという大義名分」が招いたカタストロフィーを直視できないと人類は滅ぶ

https://tokumei10.blogspot.com/2022/03/blog-post_38.html

2022年3月10日木曜日

殺し文句は　”This is about Saving Lives”

https://tokumei10.blogspot.com/2022/03/this-is-about-saving-lives.html

2021年6月24日木曜日

「ワクチンソフト」のマカフィーのマカフィーさんが★に

https://tokumei10.blogspot.com/2021/06/blog-post_77.html

、、、（爆ｗｗｗｗｗｗｗｗｗｗｗｗｗ