SARS-CoV-2 と COVID-19 に関するメモ・備忘録
良い話題と悪い話題?
米国の研究グループの動向をみているとLong COVIDはCOVID-19の後遺症ではなく、もう一つの並列しておこっているパンデミック(parallel pandemic)という位置づけなんだよね。その第一線で活躍しているのが、米イエール大学の岩崎明子教授。すごい人だなぁ、と尊敬している。 https://t.co/pLJnfo2ACm
— Hironobu SUZUKI (@HironobuSUZUKI) September 26, 2023
さすが、という感想。
米国、正攻法で、long COVID研究を推進する。 https://t.co/btHmKngEoZ— Koichi Kawakami, 川上浩一 (@koichi_kawakami) September 25, 2023
コロナ後遺症についての新知見
(Nature 2023) Yale大学のIwasaki教授らコロナ後遺症患者は総じて
(1)コルチゾール低値
(2)活性化したB細胞とサイトカイン産生T細胞
(3)スパイクに対する高い抗体価
(4)抗EBV抗体高値:ヘルペス属再活性化を示唆
であることを証明特に(1)(4)は臨床的にもすごく重要で、もしかしたら潜在性副腎不全としてのステロイド補充が症状改善に奏効するかも?
代謝内科との連携が必要ですね。
ただ、コロナウイルス持続感染やヘルペス属再活性化のリスクもあるから、一概には推奨はできないかもしれないけど。更には、コロナ後遺症を高い精度(94%)で診断するツールを開発 (ただ、マテメソ読んでもよく分からん)
→これを使いやすい形でのオンライン入力サイトが出来るといいんだけど。結果もさることながら、免疫好きにとっては馴染みの深い手法、興味深い手法盛りだくさん(対応抗原推定REAP法とか)でした。
またRを使ってのmachine learningについてもmethodで記載してあったので、将来参考にしよう。 https://t.co/BDJs8VxtIJ— Toyo@呼吸器内科専門医 (@toyosh) September 26, 2023
So pleased to report that our Mount Sinai-Yale long COVID (MY-LC) paper with @putrinolab & others is now published!! Proud of the hard work of all who contributed. We found biological signatures that can distinguish people with vs. without #longCOVID (1/) https://t.co/t8ARWBKLsQ
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
Question being asked: are there circulating cells & immune factors that are distinct in people with #longCOVID (LC) vs. those who recovered from COVID (convalescent control; CC) or those who never had COVID (healthy control; HC)? We studied 268 participants to address this. (2/) pic.twitter.com/36vrKdaZBq
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
Most participants were infected during the first wave in 2020, and studied on average about a year after the infection. Most were not hospitalized at acute phase and ~2/3 were female. We examined plasma factors, blood leukocytes & antibodies to SARS2, other viruses & self (3/) pic.twitter.com/xXGHb5Ap8S
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
Before we get to immune phenotype, the clinical symptom surveys by @PutrinoLab of these people alone were able to accurately differentiate those with vs. without long COVID with 94% accuracy. These survey instruments can be a great diagnostic tool for long COVID. (4/) pic.twitter.com/c2r1j11Z74
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
What biological factors did we find? Key findings = people with long COVID had 1) lower circulating cortisol, 2) higher activated B and cytokine-secreting T cells, 3) higher anti-Spike IgG, 4) higher EBV reactive Abs. No significant differences in # of autoantibodies. (5/) pic.twitter.com/yPjaz2s9kL
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
Machine learning identified key immune factors that can distinguish those with long COVID. These factors included lower levels of cortisol, conventional DC1, central memory T and higher levels of EBV IgG, galectin-1, APRIL…etc. (6/) pic.twitter.com/4zEMKvfafr
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
What does this mean? The study is exploratory and signal seeking, not hypothesis testing. It is a first step in identifying biomarkers that can be used in the future to diagnose long COVID. To get there, we still need to validate these markers in external cohorts. (7/)
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
What are limitations of the study? They include small sample size, only analyzed autoantibodies to exoproteome, no T cell specificity analyzed, insights from the earlier variants and may not apply to Omicron…etc. (8/)
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
What are the strengths? Deep clinical and biological phenotyping of closely and explicitly matched long COVID and control groups. External cohort validation. New insights on EBV reactivation and Th2 correlation, hormonal dysregulation suggestive of HPA axis defects. (9/)
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
This study is a result of incredible dedication and hard work by the MY-LC team, headed by Jon Klein, @wood_jamie_1 @_BlueJay3 @rahuldhodapkar @peowenlu @JeffGehlhausen @S_Tabachnikova and many others, with senior co-authors, @DavidvanDijk19, Aaron Ring & @PutrinoLab (10/) pic.twitter.com/O4UCur70Y7
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
Most importantly, we are grateful for all the participants who contributed their time, effort, blood and medical information to better understand long COVID disease pathogenesis. Very grateful to all those involved 🙏🏽 (end)
— Prof. Akiko Iwasaki (@VirusesImmunity) September 25, 2023
◆Distinguishing features of long COVID identified through immune profiling【nature 2023年9月25日】
Abstract
Post-acute infection syndromes may develop after acute viral disease. Infection with SARS-CoV-2 can result in the development of a post-acute infection syndrome known as long COVID. Individuals with long COVID frequently report unremitting fatigue, post-exertional malaise, and a variety of cognitive and autonomic dysfunctions. However, the biological processes that are associated with the development and persistence of these symptoms are unclear. Here 275 individuals with or without long COVID were enrolled in a cross-sectional study that included multidimensional immune phenotyping and unbiased machine learning methods to identify biological features associated with long COVID. Marked differences were noted in circulating myeloid and lymphocyte populations relative to the matched controls, as well as evidence of exaggerated humoral responses directed against SARS-CoV-2 among participants with long COVID. Furthermore, higher antibody responses directed against non-SARS-CoV-2 viral pathogens were observed among individuals with long COVID, particularly Epstein–Barr virus. Levels of soluble immune mediators and hormones varied among groups, with cortisol levels being lower among participants with long COVID. Integration of immune phenotyping data into unbiased machine learning models identified the key features that are most strongly associated with long COVID status. Collectively, these findings may help to guide future studies into the pathobiology of long COVID and help with developing relevant biomarkers.
Main
Recovery from acute viral infections is heterogeneous and chronic symptoms may linger for months to years in some individuals. Moreover, persistent sequelae may develop after acute infection by a number of viruses from a diverse range of viral families. Post-acute infection syndromes (PAIS) following microbial infections have also been described for over a century. Yet despite their ubiquity, the basic biology underlying PAIS development, even for extensively studied PAIS such as myalgic encephalomyelitis/chronic fatigue syndrome, remains unclear.
SARS-CoV-2 is a Betacoronavirus that is responsible for almost 7 million deaths worldwide13. Infection causes COVID-19, which can manifest as a severe respiratory disease marked by extensive immunological and multiorgan system dysfunction. Recovery from COVID-19 is often complete; however, individuals (even those with initially mild disease courses) may have increased risks for adverse clinical events and abnormal clinical findings.
In addition to developing isolated dysfunctions, some patients recovering from COVID-19 may develop a group of new onset or aggravated sequelae known as long COVID (LC). Clinically, LC presents as a constellation of debilitating symptoms including unremitting fatigue, post-exertional malaise, cognitive impairment and autonomic dysfunction, alongside other less common manifestations. These persistent sequelae markedly impair physical and cognitive function and reduce quality of life. Estimates of LC prevalence vary substantially, but prospective studies suggest that about one in eight individuals with COVID-19 experience persistent somatic symptoms that are attributable to past SARS-CoV-2 infection. Although the underlying pathogenesis of LC remains unclear, current hypotheses include the persistence of virus or viral remnants in tissues; development or aggravation of autoimmunity; microbial dysbiosis; reactivation of non-SARS-CoV-2 latent viral infections; and tissue damage caused by chronic inflammation.
To investigate the biological underpinnings of LC, a cross-sectional study was designed (Mount Sinai–Yale long COVID; hereafter, MY-LC) involving 275 participants comprising five study groups: (1) healthcare workers infected with SARS-CoV-2 before vaccination (HCW); (2) healthy, uninfected, vaccinated controls (healthy control (HC) group); (3) previously infected, vaccinated controls without persistent symptoms (convalescent control (CCs) group); (4) individuals with persistent symptoms after acute infection (LC); and (5) a second group of individuals with persistent symptoms after acute infection from an independent study (external LC, hereafter EXT-LC). Among the CC and LC groups, enrolled participants had primarily mild (non-hospitalized) acute COVID-19 and samples for this study were acquired, on average, more than a year after their acute infection. The HC, CC and LC groups underwent systematic, multidimensional immunophenotyping and unbiased machine learning of aggregated data to identify potential LC biomarkers.
コロナウイルスは心臓の動脈である冠動脈に直接感染できることがわかったというアメリカ国立衛生研究所の発表。動脈内の脂肪プラークに強い炎症を起こし、心臓発作や脳卒中のリスクを高められることが明らかになった。https://t.co/8lh0RYjqwj
— Angama (@Angama_Market) September 29, 2023
感染できない細胞がないんじゃないかと。
— Angama (@Angama_Market) September 29, 2023
>感染できない細胞がないんじゃないかと。
思わず大うけしてしまったという敗北感がいっぱいです。
— #コロナ後遺症 と #ワクチン長期副反応 と #ME/CFS の悩みを解決する窓 (@korowakunayami) September 29, 2023
◆SARS-CoV-2 infects coronary arteries, increases plaque inflammation――NIH-funded research sheds light on link between COVID-19 infection and increased risk of cardiovascular disease and stroke.【NIH(アメリカ国立衛生研究所) 2023年9月28日】
SARS-CoV-2, the virus that causes COVID-19, can directly infect the arteries of the heart and cause the fatty plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke, according to a study funded by the National Institutes of Health. The findings(link is external), published in the journal Nature Cardiovascular Research, may help explain why certain people who get COVID-19 have a greater chance of developing cardiovascular disease, or if they already have it, develop more heart-related complications.
In the study, researchers focused on older people with fatty buildup, known as atherosclerotic plaque, who died from COVID-19. However, because the researchers found the virus infects and replicates in the arteries no matter the levels of plaque, the findings could have broader implications for anybody who gets COVID-19.
“Since the early days of the pandemic, we have known that people who had COVID-19 have an increased risk for cardiovascular disease or stroke up to one year after infection,” said Michelle Olive, Ph.D., acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “We believe we have uncovered one of the reasons why.”
Though previous studies have shown that SARS-CoV-2 can directly infect tissues such as the brain and lungs, less was known about its effect on the coronary arteries. Researchers knew that after the virus reaches the cells, the body’s immune system sends in white blood cells known as macrophages to help clear the virus. In the arteries, macrophages also help remove cholesterol, and when they become overloaded with cholesterol, they morph into a specialized type of cell called foam cells.
The researchers thought that if SARS-CoV-2 could directly infect arterial cells, the macrophages that normally are turned loose might increase inflammation in the existing plaque, explained Chiara Giannarelli, M.D., Ph.D., associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine and senior author on the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaque of people who had died from COVID-19 and confirmed the virus was in those tissues. Then they took arterial and plaque cells – including macrophages and foam cells – from healthy patients and infected them with SARS-CoV-2 in a lab dish. They found that the virus had also infected those cells and tissues.
Additionally, the researchers found that when they compared the infection rates of SARS-CoV-2, they showed that the virus infects macrophages at a higher rate than other arterial cells. Cholesterol-laden foam cells were the most susceptible to infection and unable to readily clear the virus. This suggested that foam cells might act as a reservoir of SARS-CoV-2 in the atherosclerotic plaque. Having more build-up of plaque, and thus a greater number of foam cells, could increase the severity or persistence of COVID-19.
The researchers then turned their attention to the inflammation they predicted might occur in the plaque after infecting it with the virus. They quickly documented the release of molecules, known as cytokines, that are known to increase inflammation and promote the formation of even more plaque. The cytokines were released by infected macrophages and foam cells. The researchers said this may help explain why people who have underlying plaque buildup and then get COVID-19 may have cardiovascular complications long after getting the infection.
“This study is incredibly important as it adds to the larger body of work to better understand COVID-19,” said Olive. “This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID.”
Though the findings conclusively show that SARS-CoV-2 can infect and replicate in the macrophages of plaques and arterial cells, they are only relevant to the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021. The study was conducted in a small cohort of older individuals, all of whom had atherosclerosis and other medical conditions; therefore, the results cannot be generalized to younger, healthy individuals.
This work was funded by the NIH/NHLBI grants 1R01HL165258, R01HL153712, R35HL135799 and R01HL084312. NIAID and NIDDK also provided funding.
冠動脈の動脈硬化病変の特に泡沫細胞にSAR-COV2が感染しやすく、炎症反応を引き起こすということを示した論文。結構詳しく見てるよ。この論文で示されてことで気になるのはコロナウイルスが直接動脈硬化プラークの不安定性に繋がっている可能性を示す点。普通にこのデータ見て実際に体内で起ってるなら…
— Kazz.MD.Ph.D. (@KazBowen) September 29, 2023
少し論文について説明すると、まずなくなられた患者さんの心臓の冠動脈にウイルスが感染していて、Activeに増殖していることを見つけている。さらにそれが特に動脈硬化性変化が強い部分で多いことを同定。マクロファージとの相関が強いことを示している。ちなみ少し動脈硬化の説明をすると。まず動脈硬化を起こすためには血管内皮下にマクロファージが侵入(M-CSF依存で)さらにLDLが高いとそれが酸化変性を受けて酸化LDLになり、それがマクロファージに取り込まれ、マクロファージが脂肪を溜め込んで泡沫細胞と呼ばれるものに変わり、それが内皮下にPlaqueという形で存在することで動脈硬化病変ができる(SMCの増殖とかもその後起こる)だから動脈硬化病変には必ず泡沫細胞(Foam cell)が存在するし、酸化LDLを少なくするLDLの値を下げる治療が心筋梗塞を減らせるのはこのため。閑話休題
— Kazz.MD.Ph.D. (@KazBowen) September 29, 2023
この論文では更に培養したマクロファージも更に泡沫細胞化したマクロファージにもコロナウイルスが感染、増殖することも示している。幸い永続的に感染が続くわけではなく、しばらくするとウイルスそのものは排除されるわけだけど(マクロファージはそういうもん)これにともなって炎症反応を起こす(これも炎症細胞なので当たり前)
— Kazz.MD.Ph.D. (@KazBowen) September 29, 2023
ただ動脈硬化病変でこれが起こると問題で、結局動脈硬化病巣の進行にはFoam cellが引き起こす炎症が重要と考えており、もしコロナ感染がそれを、それも動脈硬化病変でおこるなら都合が悪い。この論文でも取り出してきた冠動脈に感染させても動脈硬化病変での炎症性変化が強まることは示している。
— Kazz.MD.Ph.D. (@KazBowen) September 29, 2023
ここからは少し僕の考えを書きますが、動脈硬化Plaqueの炎症は思っているよりやばいと思います。一応、心筋梗塞は元々動脈硬化病変がある人がなるわけですが、徐々に血管が狭くなって詰まるわけではないと言われています。ある程度できたPlaqueが突然やぶれること(Plaque rupture)が原因で急激に血栓ができて、冠動脈が急速に閉塞することが原因と言われています。で、なんで破れるかだけど、これよく言われるのはプラークの不安定化なんだけど、この原因は良くはわかってないけど、炎症は間違いなく一因にはなりそうと思ってます。マクロファージとか活性化されるとマトリックスを分解する酵素とか出すしね。。Fibrous capが菲薄化すれば、破れやすくなるよね〜ということでやはりコロナ感染後に心臓のEventなど血管系の急性疾患が増える理由を示した論文だと思いました。
— Kazz.MD.Ph.D. (@KazBowen) September 29, 2023
◆SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels【nature:naturecardiovascular research 2023年9月28日】
Abstract
Patients with coronavirus disease 2019 (COVID-19) present increased risk for ischemic cardiovascular complications up to 1 year after infection. Although the systemic inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques remains unknown. Here we report that SARS-CoV-2 viral RNA is detectable and replicates in coronary lesions taken at autopsy from severe COVID-19 cases. SARS-CoV-2 targeted plaque macrophages and exhibited a stronger tropism for arterial lesions than adjacent perivascular fat, correlating with macrophage infiltration levels. SARS-CoV-2 entry was increased in cholesterol-loaded primary macrophages and dependent, in part, on neuropilin-1. SARS-CoV-2 induced a robust inflammatory response in cultured macrophages and human atherosclerotic vascular explants with secretion of cytokines known to trigger cardiovascular events. Our data establish that SARS-CoV-2 infects coronary vessels, inducing plaque inflammation that could trigger acute cardiovascular complications and increase the long-term cardiovascular risk.
Main
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is uniquely marked by extraordinary tissue tropism and an array of clinical presentations, from asymptomatic infection to acute respiratory distress, multi-organ failure and death. Ischemic cardiovascular events, such as acute myocardial infarction (AMI) and stroke, due to the underlying disruption of a chronically inflamed atherosclerotic plaque, are established clinical complications of COVID-19. AMI and stroke can be triggered by several acute respiratory viral infections, including influenza virus. However, patients with COVID-19 are >7-fold more likely to have a stroke than patients with influenza, and their risk for both AMI and stroke remains high for up to 1 year after infection. The extreme inflammatory response that occurs in severe cases of COVID-19, also known as cytokine storm, is likely a contributor to the increased risk for AMI and stroke. However, the possibility that SARS-CoV-2 directly affects the coronary vasculature, as documented for other distant organs (for example, kidney, gut, brain, adipose tissue and myocardium), remains largely unexplored. In the lungs, tissue damage is aggravated by potent inflammasome activation in macrophages sensing SARS-CoV-2 virus. A similar response in macrophages infiltrating arterial vessels affected by the virus could boost plaque inflammation and risk for AMI and stroke in patients with COVID-19. Here we show, in coronary autopsy specimens from patients with COVID-19, that infiltrating macrophages were infected by SARS-CoV-2. Lipid-laden macrophages (foam cells), a hallmark of atherosclerosis at all stages of the disease, were more susceptible to SARS-CoV-2 infection than other macrophages, and this was dependent on the receptor neuropilin-1 (NRP-1). SARS-CoV-2 induced a strong pro-atherogenic inflammatory response in both macrophages and foam cells, which was largely recapitulated in an ex vivo SARS-CoV-2 infection of human vascular explants. This response may contribute to the ischemic cardiovascular complications in patients with COVID-19.
千葉県で、BA.2.86が検出される。国内ではこれで4例目のはず(東京、栃木、京都)。アメリカと中国で、日本からの渡航者からも出ていますから、もうそれなりの広がりが起こっているものとみられます。これが広がるとなかなか厄介そうです‥。https://t.co/UxTuPv2AJO https://t.co/ADrqncLCFt pic.twitter.com/j1gq5MN84o
— Takuro⚓️コロナ情報in全国/神奈川/横浜/川崎/東京/大阪/岐阜/広島/宮崎/愛知/静岡 (@triangle24) September 24, 2023
XBB 2.86検出について
ツリーhttps://t.co/qcjzjXTybI— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
XBB.2.86がドミナントになる場合、予測されるXBB.2.86 Surgeは2月前後となり、10-3rd Surgeとなる見込み。
おそらく
XBB.1.9xXBCx
XBB.2.86
の順で3つの波になると考えられる。規模はまだ不明だが、昨年BA.5ワクチンがBA.5.2 8-1st Surgeに無効であったことを念頭に置く。https://t.co/xz76UdWR0o— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
8th Surge区間のワクチン接種率
BA.5/4 WT二価ワクチンは、8th Surge終了時点で概ね70%近い人が打っている。(ノバもあるが無視しうるほど少ない)
また2022/12時点で6ヶ月内接種率は70%近い。
2022/12/1時点での2価ワクチン接種率は、25%程度。これで最高接種速度だろう。https://t.co/P3YyyLQN7e pic.twitter.com/qglICEnoIn
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
3年半、統計をずっとおってきたのでこれは断言できるが、夏のドミナント株は、秋に入ると再燃が始まる。北海道で10月冒頭、関東甲信越北陸で10月下旬。
XBBにBA.5系ワクチンは完全敗北しているが、XBBワクチンは、ハムスターやラット、マウスでは有効。
高齢者なら副反応があっても感染死よりマシ。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
ワクチン接種速度は、どんなにがんばっても10%/月を超えるのはもうあり得ない。
12月末の時点で25%が精々で、これは集団としての感染抑制効果を持たない。だから集団としては考慮する必要はない。どのみちこのワクチンの選択圧力で、21年22年同様、回避株のXBCやBA.2.86が12月には大きく伸びてくる。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
故に個人の感染リスク低減と重症化・死亡回避リスクの低減のみが目的となる。
結果として、高齢者のみが急ぎ接種すべき対象となる。これに医療従事者を加えると2千5百万人程度なので10月11月12月は、この集団で手いっぱい。
XBB1.9xなどの夏の再燃Surgeは、10月から1月。極大は11月末から年末年始。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
12月中下旬には、ワクチン回避株であるXBC, XBB.2.86, 未知の株が選択圧力によって急伸し、クリスマスごろから1月にかけて10-2nd Surgeとなる可能性がある。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
さらに、7th Surge, 8th Surge, 9th Surgeの教訓から、3月頃にはワクチン完全回避株が台頭するであろう。
これが10-3rdになるか11-1stになるかはわからない。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
ということで、
1. 医療従事者
2. 介護従事者
3. 高齢者の優先順位で疾くXBB.1.5ワクチン接種を推奨します。なお、この第一陣は、24年1~2月の時点でワクチンの有効性は消滅します。この時点では基礎免疫のかさ上げができればよい程度。
SARS-CoV-2は、ワクチン偏重ではどうにもなりません。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 24, 2023
8月1日時点で、すでにXBB.1.5はドミナント(主力株)ではない…9月中旬から始まる(始まった)抗XBB.1.5ワクチン、どこまで効果があるだろうか?🤔 https://t.co/PKIwOpoFjw
— Koichi Kawakami, 川上浩一 (@koichi_kawakami) September 25, 2023
XBB.1.5ワクチンは、XBB.1.5, XBB.1.16, XBB.1.9(EG.5), XBB.2.3には有効な様です。これらは夏のSurgeにおけるドミナントです。
10月から12月にかけて再燃します。
12月以降は、冬の株に代わり、免疫による選択圧力でワクチン回避株がドミナントになるのが21年、22年と繰り返されましたね。— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 25, 2023
今年もすでにXBCとXBB.2.86がXBB.1.5免疫回避株で国内に十分に分布していると考えられます。
22-23年シーズンの再現になると考えています。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 25, 2023
人間の免疫反応に対して春季に回避株が生まれており、さらに抗原スペクトルの狭いワクチンの運用による選択圧力で秋季以降、免疫回避株が優位になることが繰り返されています。
モグラ叩きでもモグラがパターン学習するモグラ叩きですね。
しかもワクチンによるものか免疫疲弊の兆候があります。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 25, 2023
しかも、欧米でワクチン免疫回避型変異株が出始めた頃に、日本で旧型ウイルスに対するワクチン接種が始まるという… https://t.co/zYbj6c7tXU
— Koichi Kawakami, 川上浩一 (@koichi_kawakami) September 25, 2023
治験飛ばしをしているワクチンですら対応できる変異株は発見からきっちり1年遅れで運用開始ですからね。
もうmRNAワクチンという抗原スペクトルの狭いワクチンは失敗だったというほかないです。ウイルスベクターワクチンは、ベクターを使い果たしたのでもう使えない。
人類の歴史に残る失敗ですね。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 25, 2023
生物屋さんが、ウイルスヴェクターワクチンの大規模使用は勿体無いと言っていたのを覚えていますが、ヴェクターに使えるウイルスを資源と考えれば、2年で乱獲乱掘した様なもので本来の癌や難病、エボラなどに使えるヴェクターが数種類使えなくなったことは痛恨事です。
得られたものはありますが。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 25, 2023
Sarscov2 is a neurochemical homeostasis disrupter 🧵
— Outbreak Updates (@outbreakupdates) September 28, 2023
Imagine your brain as a carefully controlled chemical reaction.
In neurodegenerative diseases like Alzheimer’s, unwanted substances (misfolded proteins) start contaminating this reaction.
Like adding sand to a finely tuned machine.
2/
— Outbreak Updates (@outbreakupdates) September 28, 2023
The spike protein from COVID-19 acts like an industrial saboteur.
He sneaks into this chemical plant and dumps more contaminating substances (amyloid fibrils) into the mix.
The more sand accumulates, the worse the machine performs.
3/
— Outbreak Updates (@outbreakupdates) September 28, 2023
What amplifies the concern is that the newly introduced abrasive particles (misfolded proteins) can engage in synergistic interactions with the pre-existing particulate matter (endogenous misfolded proteins) inside the machinery.
4/
— Outbreak Updates (@outbreakupdates) September 28, 2023
This not only compounds the mechanical wear but also catalyzes a more rapid degradation of the system’s functional integrity.
5/
— Outbreak Updates (@outbreakupdates) September 28, 2023
Lab studies indicate that this isn’t just a random act of vandalism
The spike protein is causing specific damage that accelerates the progression of conditions like Alzheimer’s and Creutzfeldt-Jakob
The saboteur knows exactly where to throw the sand to cause the most damage
6/
— Outbreak Updates (@outbreakupdates) September 28, 2023
◆SARS-CoV-2 Spike amyloid fibrils specifically and selectively accelerates amyloid fibril formation of human prion protein and the amyloid β peptide【bioRxiv 2023年9月1日】
Abstract
An increasing number of reports suggest an association between COVID-19 infection and initiation or acceleration of neurodegenerative diseases (NDs) including Alzheimer’s disease (AD) and Creutzfeldt-Jakob disease (CJD). Both these diseases and several other NDs are caused by conversion of human proteins into a misfolded, aggregated amyloid fibril state. The fibril formation process is self-perpetuating by seeded conversion from preformed fibril seeds. We recently described a plausible mechanism for amyloid fibril formation of SARS-CoV-2 spike protein. Spike-protein formed amyloid fibrils upon cleavage by neutrophil elastase, abundant in the inflammatory response to COVID-19 infection.
We here provide evidence of significant Spike-amyloid fibril seeded acceleration of amyloid formation of CJD associated human prion protein (HuPrP) using an in vitro conversion assay. By seeding the HuPrP conversion assay with other in vitro generated disease associated amyloid fibrils we demonstrate that this is not a general effect but a specific feature of spike-amyloid fibrils. We also showed that the amyloid fibril formation of AD associated Aβ1-42 was accelerated by Spike-amyloid fibril seeds. Of seven different 20-amino acid long peptides, Spike532 (532NLVKNKCVNFNFNGLTGTGV551) was most efficient in seeding HuPrP and Spike601 (601GTNTSNQVAVLYQDVNCTEV620) was most effective in seeding Aβ1-42, suggesting substrate dependent selectivity of the cross-seeding activity.
Albeit purely in vitro, our data suggest that cross-seeding by Spike-amyloid fibrils can be implicated in the increasing number of reports of CJD, AD, and possibly other NDs in the wake of COVID-19.
Introduction
Amyloids and viruses are each notorious for their detrimental effect on human health. There are also many ways in which cross-talk between these two disease causing entities resulting in increasing risk of harm to the host. Several neurodegenerative diseases (NDs) are intimately related to misfolding and amyloid formation of endogenously expressed proteins. However, research has to date failed to describe why some but not others fall victim to these diseases. In a retrospective study of 800 000 individuals from biobanks in Finland and the UK it was evident that infection from some of our most common viruses, e.g. Influenza and Herpes zoster was connected to an increased risk of some of the most common NDs such as Alzheimer’s disease (AD) and Parkinson’s disease (PD).
The neurological manifestations of COVID-19 both in the acute phase and as long term sequel of SARS-CoV-2 infection have been widely observed and described during the COVID-19 pandemic. The dominating explanation for this is neuroinflammation. Neuroinflammation is a common denominator of NDs. The specific roles of neuroinflammation in prion disease was recently reviewed.
NDs are specifically associated with the misfolding and amyloid formation of intracerebral proteins. AD is linked to formation of extracellular amyloid plaques with the Aβ peptide as main constituent and intracellular neurofibrillary tangles composed of Tau protein. Prion diseases are caused by the misfolding and aggregation of the prion protein, PrP, that is abundant on the extracellular surface of all neuronal cells in mammals. Although each distinct disease is associated with its own set of misfolded proteins, more and more evidence is pointing towards the possibility of cross-seeding, that is that amyloids formed of one type of protein can induce amyloid formation of another protein.
Several SARS-CoV-2 proteins are known to form amyloid. The proteins translated from viral open reading frame genes (ORFs) are often intrinsically disordered and/or fold only in the context of the viral particle. SARS-CoV-2 ORF6 and ORF10 are amyloidogenic and the resulting amyloids exhibit neurotoxic properties on cultured cells. Nucleocapsid proteins (NCAPs) are crucial for the assembly of viral particles. These proteins contain low complexity domains that are important for the self-assembly of the virus particle but the complementarity between adjacent polypeptide chains can also promote the formation of amyloid structure. The low complexity domain of SARS-CoV-2 NCAP forms amyloid in vitro and this amyloid was recently suggested as a drug candidate for treatment of COVID-19.
The SARS-CoV-2 Spike proteins forms amyloid when cleaved by neutrophil elastase. Elastase is abundant in covid induced inflammation. Amyloid derived from SARS-CoV-2 spike protein has the potential to hamper fibrinolysis of seeded fibrin and hence might be one explanation for microclot formation in severe and long COVID-19. Data from Brogna and colleagues demonstrate that Spike protein produced in the host as response to mRNA vaccine, as deduced by specific amino acid substitutions, persists in blood samples from 50% of vaccinated individuals for between 67 and 187 days after mRNA vaccination. Such prolonged Spike protein exposure has previously been hypothesized to stem from residual virus reservoirs, but evidently this can occur also as consequence of mRNA vaccination.
Other viruses from different families comprise amyloidogenic proteins. As an example, several proteins of Influenza A, causing seasonal flu, are known to be amyloidogenic. Recombinant expressed Pb1-F2 protein forms amyloid in vitro and in experimentally infected cells. Influenza A non-structured protein 1 (NS1) can also from amyloid in vitro. Influenza A infection has been shown to induce misfolding of PrP.
During the past 3 years, several case reports of Creutzfeldt-Jakob disease (CJD) manifestation in parallel with COVID-19 infection or vaccination have been published. Recently it was suggested by Stefano et al that the conversion of PrPC to PrPSc and the subsequent mitochondrial dysfunction should be considered when addressing the etiology of long COVID-19.
Although AD is a very slowly progressing disease, there are already indications that suggest a connection between COVID-19 infection and downstream risk of AD. Brain atrophy was prevalent in patients infected post COVID-19 for early strains. Aβ aggregates were found postmortem in brains of young COVID-19 infected patients. COVID-19 imposed 1.69 increased risk for new diagnosis of AD within 360 days at age >65 years.
A recent in vitro study showed augmented Aβ1-42 fibril formation induced by preformed seeds from SARS-CoV-2 Spike-protein peptide 1058-1068. We herein follow up the concept of cross-seeding of ND proteins with SARS-CoV-2 Spike amyloid fibrils. Cross-seeding is a testable hypothesis and we addressed it in our well-established in vitro seeding assays by cross-seeding of human prion protein and Aβ1-42 peptide with seven different amyloid fibrils from peptides of the SARS-CoV-2 spike protein.
今から3ヶ月後、今年の年末年始の主役はBA.2.86です。 https://t.co/L0jhKZuI7f
— ramos2 (@ramos262740691) September 28, 2023
Here's an animated map showing the spread of the new BA.2.86 "Pirola" variant.
152 samples have been reported so far, over 5 continents.
Locations are approximate – typically country and state/province.
🧵 pic.twitter.com/3EgzMijVMj— Mike Honey (@Mike_Honey_) September 20, 2023
Here's another animated map showing the spread of the new BA.2.86 "Pirola" variant across Europe.
105 samples have been reported so far, mostly from the UK (49), Denmark (17) and Sweden (15).
Locations are approximate – typically country and state/province. pic.twitter.com/8ukVjf6TAh
— Mike Honey (@Mike_Honey_) September 20, 2023
Here's another animated map showing the spread of the new BA.2.86 "Pirola" variant across North America.
19 samples have been reported so far, mostly from the US (16).
Locations are approximate – typically country and state/province. pic.twitter.com/YZNbWH2ibs
— Mike Honey (@Mike_Honey_) September 20, 2023
The first sub-lineage has been designated: BA.2.86.1, featuring the Orf1a:K1973R mutation.
BA.2.86.1 is more prevalent in Europe, notably the UK, Denmark and Sweden. pic.twitter.com/epYeDOmhbJ
— Mike Honey (@Mike_Honey_) September 20, 2023
As the BA.2.86.1 designation has not yet flowed through to Nextclade, I'm approximating it here by searching for samples with the characteristic mutations.
This method catches 122 of the 152 BA.2.86.* samples, so a clear majority.
— Mike Honey (@Mike_Honey_) September 20, 2023
Interactive genomic sequencing dataviz, code, acknowledgements and more info here:https://t.co/G28yjjtX4V
Interactive mutation matching dataviz, code, acknowledgements and more info here:https://t.co/7QMeNDBXWd
🧵 end
— Mike Honey (@Mike_Honey_) September 20, 2023
統計分析者としてこの見解を支持します。
XBCの挙動にもよりますが、XBB.2.86は、遅くとも24年1月から2月にかけて極大期を取る10-3rd Surgeのドミナントとなる見込みです。10-1st Surgeは、EG.5xで、現在発生した可能性あり。11月が極大。
10-2nd SurgeとしてXBCを見込み、これが12~1月極大。 https://t.co/MDJtauFDiw
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 28, 2023
XBCがたいしたことなければ、XBB.2.86が繰り上がる形で10-2nd Surgeを形成し、年末年始から2月にかけてのSurgeとなる見込み。
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 28, 2023
9/19の第一の秋の冷え込みで北海道、東北、甲信越北陸全域と、中国以東の標高の高い地域でEG.5.x 10-1st Surgeが発生した兆候があります。
現在、重点的に追跡中です。
今打てば、1月にもほぼ無効となりますが、北海道東北甲信越北陸関東では、ワクチン接種の検討推奨。https://t.co/QQ1feJMn4U
— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 28, 2023
インパクトある新結果(Clinical Infectious Diseases)
新型コロナ感染でのウイルス量のピークと抗原検査
22年4月-23年4月施行
・ウイルス量の中央値は発症日から上昇し「4/5日目にピーク」
・抗原検査の感度も発症1日目は30-60%、4日目で80-93.3%発症時にウイルス量が高かった以前と異なると指摘
— 大津秀一🍀医師🍀緩和ケア内科🍀早期からの緩和ケア外来🍀院長🍀「どこでも緩和®」で全国対応可 (@shuichiotsu) September 28, 2023
この結果より、症状発症から最低4日目迄は(感染していても陰性と出る場合も相応にある事から)マスクを用いて他者にうつさないようにする必要ありと研究者は指摘
また2日目がピークのインフルよりも遅いと発見
症状ある場合の感染対策の重要性が強調される結果
— 大津秀一🍀医師🍀緩和ケア内科🍀早期からの緩和ケア外来🍀院長🍀「どこでも緩和®」で全国対応可 (@shuichiotsu) September 28, 2023
新型コロナは発症してまもなくや前後が一番うつしやすいという理解を、今は異なると改めて修正する結果
発症早期に抗原検査で陽性にならない場合も相当ある事も改めて示す
症状ある場合は5日目位はうつさない配慮を特に厳重に講じる必要ありそう
経時的にウイルスの性質等も変わるのを実感する結果
— 大津秀一🍀医師🍀緩和ケア内科🍀早期からの緩和ケア外来🍀院長🍀「どこでも緩和®」で全国対応可 (@shuichiotsu) September 28, 2023
第9波では、抗原検査の陽性化が遅れるのはEG.5と派生株の特徴かもしれないと言われていましたが、それ以前から傾向はあったのですね。感染性の推移が気になるところです。ウイルス排出量が発症後にピークに向かうとすれば、有症状者がしっかり療養すれば有効な対策になるわけですが・・・。
n
— FORCEPS (@FORCEPS4) September 28, 2023
仰る通りで、私も以前から傾向があったと示されたことには驚きました。
本年4月までの研究なので、EG.5等を主対象として研究が行われると、さらにこの方向性が強まった結果が出る可能性もあるかもしれません。
そしてまさしく、感染後の対策と期間が問われていると示す結果でもありますが・・。
— 大津秀一🍀医師🍀緩和ケア内科🍀早期からの緩和ケア外来🍀院長🍀「どこでも緩和®」で全国対応可 (@shuichiotsu) September 28, 2023
まったく周知徹底されていないですよね。
内閣感染症危機管理統括庁は今は平時との認識とのことですし、どこがどう動けばこのような必要な情報が世の中に届くのかということが現状見えづらくなってしまっていますよね。
やらないよりは良いと思って、個人での発信は続けていますが。
— 大津秀一🍀医師🍀緩和ケア内科🍀早期からの緩和ケア外来🍀院長🍀「どこでも緩和®」で全国対応可 (@shuichiotsu) September 28, 2023
衰退産業と言われつつも、いまだにテレビの影響力が大きいのを感じます。アナウンサー等の「コロナが明けて」は本当に迷惑しています。
— FORCEPS (@FORCEPS4) September 28, 2023
子供に特化した研究がほしいところですが、この結果はとても重要だと思います。
感染症状があっても早期に感染対策を解除する傾向が強まったことも、今波で感染の収束が遅くなったことの原因の一端は提供しているかもしれません。
— 大津秀一🍀医師🍀緩和ケア内科🍀早期からの緩和ケア外来🍀院長🍀「どこでも緩和®」で全国対応可 (@shuichiotsu) September 28, 2023
これはちょっと認識を改めないと…
コロナの特徴だった発症前のウイルス量ピークの概念が変わる「新型コロナは発症してまもなくや前後が一番うつしやすいという理解を、今は異なると改めて修正する結果」
「発症早期に抗原検査で陽性にならない場合も相当ある事も改めて示す」… https://t.co/mMk5so7Tzb— 伊賀 治 (@osamu_iga) September 28, 2023
合唱祭練習が続くが、ノーマスクの生徒が多い中、授業中毎度うるさいくらいに言うのは、「(全員マスクが安全だが、せめて)風邪様症状ある場合、そして濃厚接触者である場合、療養後すぐの人はマスクね!」と。すると、眼の前の生徒が療養直後(6日目)でノーマスクの子だった。(危ない、、)→
— アポロ小太郎 (@lustigmusik) September 28, 2023
自分で「えっ?!あ、じゃオレ、、」と言ったので、「お、言えて偉いね、先生、カッコいいマスク持ってるよ」と言うと「つけてみたい!」と。そうすると、もう一人自分濃厚接触者という子が出てきて「自分も欲しい」と。クラスターゼロ、罹患者ゼロで全員で舞台立ちたいよね、そのためにできること→
— アポロ小太郎 (@lustigmusik) September 28, 2023
2週間感染者無し、濃厚接触者無し(ここは難しいが)、療養後はマスク、これなら、かなり安全に本番迎えられるよ!そう言ってます。それで申し出が出たのは良かった。その事を担任に告げると(万一の親からのクレーム対応用)、なんとそのクラス、面々と感染連鎖が続いているとのこと。→
— アポロ小太郎 (@lustigmusik) September 28, 2023
一度に数人出ればクラスターで学級閉鎖だが、順々に出てると、、、療養後6日目には登校でノーマスクだから当然😱 いやいや、これは非常にまずいことになってるじゃないか😤 担任も一学期最後の方で罹患。この先生は5類以後も唯一ずっとマスクしていて、クラスの状況を非常にまずいと思っているが、、
— アポロ小太郎 (@lustigmusik) September 28, 2023
〉療養後6日目には登校でノーマスクだから当然😱
これ、10日目までノーマスク駄目って指導する義務が学校にはあるんです。文科省通知で。 https://t.co/O4ym3IBnzj
— vogelsang7 (@vogelsang7) September 28, 2023
本来、発症10日目までマスク外す指導はできないですから、マスク外さなければならない教育活動は見学にする体制をとるべきです。
そして発症6日目に熱中症リスクあるほどの体育は医師として勧められません。— vogelsang7 (@vogelsang7) September 29, 2023
発症10日目までマスク外してリコーダーさせる教育指導はできないはずです。文科省の通知では。それをするには新たな文科省通知が必要なはず。
文科省への疑義紹介案件ですね。— vogelsang7 (@vogelsang7) September 29, 2023
発症10日目までマスク着用を推奨するという学校の義務(施行規則改正通知2023/4/28)が学校現場で忘れられていますね。 https://t.co/kkeNk2CHjV
— vogelsang7 (@vogelsang7) September 28, 2023
発症10日目までマスク着用を推奨するという学校の義務(施行規則改正通知2023/4/28)が学校現場で忘れられていますね。 https://t.co/kkeNk2CHjV
— vogelsang7 (@vogelsang7) September 28, 2023
😥やれやれ
BA.2.86.1亜系がすでに(L455S)に変異を持っているそうで、今のところまだ4つの配列(4カ国のもの)しかないけれど、これからもっと増えるだろうと。
これはほぼ間違いなくトップクラスのエスケープ変異 https://t.co/Fr4HWfzo8V
— yumi ゆみ (@ygjumi) September 27, 2023
455Sを獲得したBA.2.86.1-derivativeは、現在、呼称が変更されている: JN.1https://t.co/R65iTqQ9D5
— yumi ゆみ (@ygjumi) September 29, 2023
わかりやすい図
BA.2.86.1+455Shttps://t.co/f7m8RXqmXe— yumi ゆみ (@ygjumi) September 29, 2023
Keeping track of which new designations are related to BA.2.86 Pirola is going to be confusing.
The other variants are very genetically similar to each other, Pirola stands alone.
Does JN.1 sound related to BA.2.86?
That's why the Pirola name umbrella is needed here. pic.twitter.com/OZGOVu6d2X
— JWeiland (@JPWeiland) September 29, 2023
JN.1 (= BA.2.86.1.1 = B.1.1.529.2.86.1.1)https://t.co/vDDcIzGxNM
— yumi ゆみ (@ygjumi) September 29, 2023
NIH: SARS-CoV-2 は冠動脈に感染する可能性があります。
SARS-CoV-2 は心臓の動脈に直接感染し、動脈内の脂肪プラークに高度な炎症を引き起こし、心臓発作や脳卒中のリスクを高めます。 https://t.co/HOQWi6knwU
— R連続体 MT Ph.D D.H.Sc. (@Rrenzokutai) September 28, 2023
あれだけ循環器系を攻撃するものね。
Fluでこんなの聞いたことない。— Hiroshi Makita Ph.D. 誰が日本のコロナ禍を悪化させたのか?扶桑社8/18発売中 (@BB45_Colorado) September 28, 2023
Mysterious Pediatric hepatitis of unknown etiology,
➡️We were right, it was COVID-19!
T Cell Cross-reactivity in Autoimmune-like Hepatitis Triggered by COVID-19https://t.co/VcTTVCzvw2 pic.twitter.com/BHxvRaq5Ck
— Harry Spoelstra (@HarrySpoelstra) September 30, 2023
T cells are intelligence agents and SARS-CoV-2 is a foreign spy using stealth tech.
The virus tricks the T cells by mimicking a liver cell protein.
The good guys can’t tell friends from enemies, causing collateral damage like autoimmune-like hepatitis. https://t.co/opneWXL3BI
— Outbreak Updates (@outbreakupdates) September 30, 2023
It’s like a spy using advanced stealth technology, exploiting security vulnerabilities within the hepatocytes by mimicking one of their own proteins (ABCD3).
— Outbreak Updates (@outbreakupdates) September 30, 2023
◆T cell cross-reactivity in autoimmune-like hepatitis triggered by COVID-19【ScienceDirect 2023年9月28日】
Over 1000 cases of pediatric hepatitis of unknown etiology have been reported worldwide since the first case was reported in the UK. To date, the etiology of pediatric hepatitis remains unknown and controversial. Adenovirus was first suspected to be the cause as it was present in the blood samples of the majority of cases. Partial cases have also been tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, it is still unclear how these viruses contribute to pediatric hepatitis. In the case of a pediatric patient with SARS-CoV-2 infection, the liver biopsy showed acute submassive hepatocyte necrosis, accompanied by a significant increase in T cell infiltration. Furthermore, CD8+ T cell dominant hepatitis induced by coronavirus disease 2019 (COVID-19) vaccination has also been recently reported. Although it is known that T cell receptors (TCRs) can discriminate between self- and non-self-antigens, it is now well-accepted that TCRs exhibit cross-reactivity toward similar and even distinct antigen peptides. Thus, we hypothesized that following SARS-CoV-2 infection or vaccination, T cells carrying TCRs that recognize self-antigens undergo clonal expansion, which could eventually result in the onset of autoimmune-like hepatitis.
10月からの医療体制についての説明会を聞いた。酷すぎる。過去最大の第7波を超えたとしても、入院病床は当時の半数以下。それ以上は決して増やさない。例えば骨折の方がコロナ感染しても整形外科病棟で入院させる。とにかく全診療科で受け入れるようにと。説明している人もできるわけないと
— くぅ (@itsukainuakani) September 29, 2023
分かりきっているような内容に言葉を失う。どこの病院でも診るようにと言うのに、医療点数はあり得ないほど削られる。4月には他の病気と同じ扱いになる見込みだって(謎)コロナ患者を受け入れてくれている心ある開業医の先生方は本当にキツイと思う。
— くぅ (@itsukainuakani) September 29, 2023
要するに:
岸田文雄「支援は全て打ち切るが、一般病棟でコロナ患者を受け入れろ。クラスターが発生したら病院が責任を取れ、俺の知ったことじゃない」 https://t.co/oeWXWJoRlp— FORCEPS (@FORCEPS4) September 29, 2023
要するに:
電車で隣になったおばあちゃんの人生と基礎疾患について想像できないまだ青い若造で埋め尽くされたハロウィンの電車だけではなく。
一般病棟も高齢者殺しの姥捨山と化す。
どうオペレーションできるか。一般病棟も鬼換気するしかねぇな。冬来るけどhttps://t.co/W4yH2Jn4pK— ramos2 (@ramos262740691) September 30, 2023
「基礎疾患?コロナ怖い?じゃ家にいろよw」と今は笑っている若者へ
人生は長く、貴方もいずれ必ず基礎疾患持ちになります。それは初めから確定している未来です。そしてその時でもコロナは消え去っていないこと、僕が保証します。
貴方が貴方の未来を嘲笑うのを、いつか辞めてくれることを願います
— ramos2 (@ramos262740691) September 30, 2023
ちなみに昨日夏休みが終わったのは、おそらく昨日、BA.2.86が獲得してはいけない変異を1つ獲得し、さらに一段階上に上がったからです。書き忘れた。てへ
— ramos2 (@ramos262740691) September 29, 2023
問題の子は、JN.1と名付けられた模様です。https://t.co/CBoKDIzywY
— ramos2 (@ramos262740691) September 30, 2023
Pirola with the potentially important escape mutation 455S has been designated JN.1
It was actually lined up to be JP.1, but due a mistake in skipping JN designation earlier in the week, Pirola is now JN.1
Really glad it's not JP.1, the naming conspiracies would have been nuts!
— JWeiland (@JPWeiland) September 29, 2023
BA.2.86.1、獲得しちゃったよね。https://t.co/WYqLdl8BY6
— yumi ゆみ (@ygjumi) September 29, 2023
一部の研究者たちの「最悪の想定」ワーストケースは、新型コロナにおいては8割当たってきました。これまで。
なので、今回も最悪と思ってる部位に変異追加したこれが広がるのはほぼ確かなと思ってます。
— ramos2 (@ramos262740691) September 29, 2023
BA.2.86* #Pirola updates
Total sequences: 287 (+29)
Today's updates include seqs from: #SouthAfrica, #Spain, #England, #CanaryIsland, #Australia
https://t.co/uCBhVnhF8a pic.twitter.com/CYKDZGMnTM— Raj Rajnarayanan (@RajlabN) September 29, 2023
変異がいかに厄介か。21年末には、2回接種で獲得した中和抗体が効かないオミクロン株(BA.1)が出現した。22年末には、どんな中和抗体もほぼ効かないXBB系統が出現した(今主流のEG.5もXBB系統)。突如登場したBA.2.86はこれと並ぶ3度目の出来事か、あるいは別の出来事が起こるか‥https://t.co/R3NwGwUi7m
— Takuro⚓️コロナ情報in全国/神奈川/横浜/川崎/東京/大阪/岐阜/広島/宮崎/愛知/静岡 (@triangle24) September 30, 2023