• Long COVID is associated with severe cognitive slowing: a multicentre cross-sectional study - eClinicalMedicine
    https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(24)00013-0/fulltext
    https://www.thelancet.com/cms/asset/eaa00ef2-1f2b-47e6-aa79-cc4f03bfae4d/gr2.jpg

    Summary
    Background
    COVID-19 survivors may experience a wide range of chronic cognitive symptoms for months or years as part of post-COVID-19 conditions (PCC). To date, there is no definitive objective cognitive marker for PCC. We hypothesised that a key common deficit in people with PCC might be generalised cognitive slowing.
    Methods
    To examine cognitive slowing, patients with PCC completed two short web-based cognitive tasks, Simple Reaction Time (SRT) and Number Vigilance Test (NVT). 270 patients diagnosed with PCC at two different clinics in UK and Germany were compared to two control groups: individuals who contracted COVID-19 before but did not experience PCC after recovery (No-PCC group) and uninfected individuals (No-COVID group). All patients with PCC completed the study between May 18, 2021 and July 4, 2023 in Jena University Hospital, Jena, Germany and Long COVID clinic, Oxford, UK.
    Findings
    We identified pronounced cognitive slowing in patients with PCC, which distinguished them from age-matched healthy individuals who previously had symptomatic COVID-19 but did not manifest PCC. Cognitive slowing was evident even on a 30-s task measuring simple reaction time (SRT), with patients with PCC responding to stimuli ∼3 standard deviations slower than healthy controls. 53.5% of patients with PCC’s response speed was slower than 2 standard deviations from the control mean, indicating a high prevalence of cognitive slowing in PCC. This finding was replicated across two clinic samples in Germany and the UK. Comorbidities such as fatigue, depression, anxiety, sleep disturbance, and post-traumatic stress disorder did not account for the extent of cognitive slowing in patients with PCC. Furthermore, cognitive slowing on the SRT was highly correlated with the poor performance of patients with PCC on the NVT measure of sustained attention.
    Interpretation
    Together, these results robustly demonstrate pronounced cognitive slowing in people with PCC, which distinguishes them from age-matched healthy individuals who previously had symptomatic COVID-19 but did not manifest PCC. This might be an important factor contributing to some of the cognitive impairments reported in patients with PCC.

  • Mortalité cardiovasculaire des 20-49 ans aux USA 🇺🇸 (CDC)... C-A GUSTAVE

    https://threadreaderapp.com/thread/1693270068820344843

    1/12
    Je voudrais profiter du thread cité 🔽 pour clarifier un point qui est trop souvent caricaturé par les « rassuristes » ou les « sophistes du tout ou rien ».
    Ci-dessous vous avez les données de mortalité cardiovasculaire des 20-49 ans aux USA 🇺🇸 (CDC)...

    2/12
    On peut dire ce qu’on veut à propos de la « bénignité » de la covid, les données épidémio sont têtues :
    son émergence est associée à une nette cassure ↗️↗️ de cette mortalité chez des gens pourtant présentés comme « non vulnérables » dans les narratifs dominants...
    3/12
    Vous pouvez également voir que cette ↗️↗️ n’a rien à voir avec la vaccination, puisqu’elle apparaît AVANT, et ↘️ APRÉS, mais sans revenir au niveau pré-pandémique.
    De plus, en prévision des commentaires habituels, je vous renvoie d’emblée à l’étude suivante...
    4/12
    Sur >4 MILLIONS de patients suivis sur 12 mois, tous NON-vaccinés, l’issue clinique la fortement ↗️ au décours d’une infection par SARS-CoV-2 est... la myocardite !...

    https://twitter.com/IanCopeland5/status/1626576433920212992?s=20

    5/12
    Apparemment, l’info est peu connue, pourtant elle est documentée depuis début 2021.
    Le CDC retrouvait un risque de myocardite 16x plus élevé chez les personnes avec un antécédent de covid, et très loin devant le sur-risque associé à la vaccination
    Association Between COVID-19 and Myocarditis...
    Viral infections are a common cause of myocarditis. Some studies have indicated an association between COVID-19 and myocarditis.
    https://www.cdc.gov/mmwr/volumes/70/wr/mm7035e5.htm
    6/12
    Que disent les rassuristes/sophistes face à de tels threads ?
    « ah le retour des histériques », « agitateurs de peurs », « covido-dingo », « ça y est on va tous mourir 🤪 »... et j’en passe.
    La question n’est pas là du tout, et c’est justement là toute la tartuferie de leur propos
    7/12
    Reprenez ce graphe 🔽
    Regardez l’écart entre le niveau pré-pandémique et la nouvelle médiane induite par la pandémie.
    Cet écart c’est le « nouveau normal » qui va imposer des réajustement socio-économiques majeurs... Image
    8/12
    Cet écart, c’est une morbi-mortalité qu’on n’avait pas avant, et qui va perdurer désormais avec la persistence du virus et des cycles de réinfections.
    Ce sont donc des dépenses de santé en plus, une charge supplémentaire sur le système de santé...
    9/12
    Ce sont également des difficultés individuelles supplémentaires (une myocardite virale peut finir en insuffisance cardiaque et donc en invalidité). Ce sont également bien plus d’arrêts maladies « nouveaux » par rapport à l’avant-pandémie...
    10/12
    Bref, et là ce n’est qu’un exemple parmi tous les équilibres épidémio-démographiques qui vont être réajustés par le « vivre avec » associé à l’abandon de toute mesure de prévention des infections.
    Il ne s’agit pas de dire « on va tous mourir », c’est plus que ridicule...
    11/12
    Il s’agit simplement de vous rappeler que ce graphe vous montre que c’est facile de détourner le regard du danger, mais ça n’élimine pas le danger.
    Son impact va imposer des réajustement socio-économiques, et c’est peu probable qu’ils vous plaisent.
    12/12
    Comme toujours, ce n’est pas de l’alarmisme, c’est juste un thread de plus pour nous remettre tous collectivement face à nos responsabilités.
    Comme veut l’adage, on récolte ce qu’on sème.

  • Long-term cardiovascular outcomes in COVID-19 survivors among non-vaccinated population: A retrospective cohort study from the TriNetX US collaborative networks - eClinicalMedicine
    https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370%2822%2900349-2/fulltext

    From a cohort of more than 42 million records between 1 January 2019 and 31 March 2022, a total of 4,131,717 participants who underwent SARS-CoV-2 testing were recruited.

    (...)

    The COVID-19 survivors were associated with increased risks of cerebrovascular diseases, such as stroke (HR [95% CI] = 1.618 [1.545-1.694]), arrhythmia related disorders, such as atrial fibrillation (HR [95% CI] = 2.407 [2.296-2.523]), inflammatory heart disease, such as myocarditis (HR [95% CI] =4.406 [2.890-6.716]), ischemic heart disease(IHD), like ischemic cardiomyopathy (HR [95% CI] = 2.811 [2.477-3.190]), other cardiac disorders, such as heart failure (HR [95% CI] =2.296 [2.200-2.396]) and thromboembolic disorders (e.g. pulmonary embolism: HR [95% CI] =2.648 [2.443-2.870]).

    (...)

    Des commentaires ?

  • Covid-19 : les formes sévères provoqueraient une baisse du QI
    https://www.tf1info.fr/sante/covid-19-les-formes-severes-provoqueraient-une-baisse-du-qi-selon-une-etude-

    D’après les scientifiques de l’Université de Cambridge et de l’Imperial College de Londres, dont les travaux ont été publiés dans la revue eClinicalMedicine de The Lancet, les formes graves du Covid-19 entraîneraient des troubles cognitifs similaires à 20 ans de vieillissement, entre 50 et 70 ans. Soit l’équivalent, selon l’Imperial College, d’une perte de dix points de quotient intellectuel (QI).

    Multivariate profile and acute-phase correlates of cognitive deficits in a COVID-19 hospitalised cohort
    https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00147-X/fulltext

    On average, the scale of deficits was most similar to that observed in normal cognitive decline between the ages of 50–70; however, when examined in more detail the pattern of cognitive deficits was most pronounced for different tasks than either age-related decline or the dementia group. These more detailed results highlight the potential value of cross comparing multivariate profile of COVID-19 cognitive deficits to a wider variety of populations in order to identify potential similarities to other neurological conditions. Future work should also expand the repertoire of disorders, especially populations who have recovered from other critical illnesses, and cross relate these detailed cognitive profiles to imaging and blood biomarker measures of neuropathology and tracking recovery and decline trajectories over a longer temporal scale.

    In summary, severe COVID-19 illness is associated with significant objectively measurable cognitive deficits that persist into the chronic phase. The scale of the deficits correlates with clinical severity during the acute phase as opposed to mental health status at the time of assessment, shows at best a slow recovery trajectory and the multivariate profile of deficits is consistent with higher cognitive dysfunction as opposed to accelerated ageing or dementia.

    Ça donne vraiment envie de l’attraper comme tout le monde.

  • Pourquoi vous devriez conserver le masque en intérieur - JustPaste.it
    https://justpaste.it/1rxvu

    Sous prétexte que la majorité des adultes ont reçu 2 ou 3 doses de vaccin, les gouvernements ont décrété un peu partout la fin de la pandémie et referment la parenthèse interventionniste qui allait avec.
    3. Du fait de cette capitulation totale des pouvoirs publics face à la circulation de SARS-CoV-2, vous allez être beaucoup plus exposé à l’infection que lors de la phase pré-vaccinale de la pandémie, avec une menace croissante pour votre santé.
    4. Or, quel que soit le baratin « rassuriste » en vogue, SARS-CoV-2 reste un pathogène dangereux. Dans une simple optique de préservation de votre santé, vous devriez essayer d’éviter l’infection autant que possible.

    • Et donc merci à « Maître Pandaï » qui, soit dit en passant, est un twittos remarquablement organisé qui réussit le tour de force de se référer à des tweets d’il y a plusieurs mois (dont les siens). Sans parler des nombreuses sources citées en exemple. Ce thread de 108 posts témoigne d’un argumentaire sans faille. Je suis toujours admiratif de ces personnes qui ont une telle puissance de travail et d’organisation.

      Ceci dit, il y a sûrement des outils sur la plateforme qui permettent une telle organisation des infos mais j’ai jamais vraiment pris le temps de creuser.

      Source : https://twitter.com/Panda31808732/status/1502747054979923970

    • Tentons un condensé des affirmations importantes, sans les preuves et détails :
      – Il faut garder un masque FFP2 partout en intérieur et aérer fortement.
      – Le virus continue de circuler fortement, partout.
      – C’est un virus AÉROSOL, en intérieur vous le chopez même loin des gens, et même si les gens qui l’ont expiré dans la pièce sont déjà partis ! Il ne faut donc pas DU TOUT respirer l’air intérieur sans masque filtrant fort (FFP2).
      – Les vaccins actuels sont moins efficaces et moins longtemps contre les variants du moment donc il FAUT se protéger de manière non pharmaceutique : masques + aération.
      – Le vaccin est un airbag ou ceinture : ça amortit le choc mais ça ne rend PAS les accidents (l’infection) désirables.
      – Tout le monde s’est focalisé sur les cas graves (hopital) et les décès, alors qu’on peut TOUS finir avec un covid long = des maladies chroniques handicapantes. Même celleux qui sur le moment ont juste eu le nez bouché. Même chez les jeunes, même celleux en bonne santé.
      – Le covid long, les maladies chroniques handicapantes, c’est le PRINCIPAL RISQUE quand on attrape le covid !
      – Le covid est une maladie SANGUINE (vasculaire, des vaisseaux sanguins) : elle peut toucher le corps entier, poumon, cerveau, cœur, reins, articulations, TOUT.
      – Une fois infecté, risque augmenté pour : insuffisance respiratoire, hypertension, démence, diabète, insuffisance rénale, maladies cardiovasculaires, AVC, embolie pulmonaire… Et ce risque augmente à CHAQUE infection.
      – Quand on est vacciné : minimum 10% de risque de finir avec des maladies chroniques, 1 fois sur 10, c’est beaucoup. Et c’est plus quand on n’est pas vacciné.
      – Or on peut être infecté des DIZAINES de fois dans notre vie : en moyenne 1 à 2 fois par an chacun, et à CHAQUE infection on aura un risque élevé de finir avec des maladies chroniques.
      – Le covid, ce n’est pas « ce qui ne me tue pas me rend plus fort » mais « ce qui ne me tue pas peut quand même bousiller ma santé, puis mute et réessaye quelques mois plus tard ».
      – Si on échappe aux handicaps la 1ère infection, la 2ème… c’est peu probable d’y échapper à chaque fois sur les dizaines de fois où on peut être infecté le reste de notre vie. Et une fois qu’on est en mode maladies chroniques, c’est handicap à vie.
      – Les plus pauvres attrapent plus le covid => le covid augmente énormément les maladies chroniques handicapantes => qui empêchent de travailler correctement ensuite => le covid rend plus pauvre => cercle vicieux.
      – Il FAUT donc se protéger au max, pour ne jamais le choper.
      – Faire chacun des gestes ne suffit pas : il faut militer pour une politique publique gouvernementale : FFP2 gratuits, travaux d’aération des lieux publics (à commencer par l’école, nid du virus depuis le début), etc.

      Les deux schémas les plus importants :

    • Autres arguments qui confortent la thèse que le Covid n’est pas une « grippette » mais que le virus #SARS-CoV2 attaque le système vasculaire, ce qui pourra générer des symptômes diversifiés ainsi que des séquelles durables et dévastatrices.

      31. Ce papier sur le Covid long décrit plus de 200 symptômes différents à travers tout le corps. Les plus courants dans l’étude étaient : fatigue, malaise post-effort, dysfonctionnements cognitifs.
      https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00299-6/fulltext

      32. Le Covid est une maladie vasculaire : « on observe une atteinte des cellules qui tapissent l’intérieur de la paroi des vaisseaux sanguins. Cette fine couche de cellules qui forme le revêtement interne des vaisseaux porte le nom d’endothélium. »
      https://www.lemonde.fr/blog/realitesbiomedicales/2020/04/29/covid-19-est-aussi-une-maladie-inflammatoire-vasculaire (article du 22/04/2020 ... Ah oui, déjà ?)

      32b. « Envisager la Covid-19 comme une maladie endothéliale permet en outre de rendre compte de la variété des symptômes observés dans cette pathologie multi-cibles, qui n’atteint pas seulement les poumons, mais également le cœur, les vaisseaux, les reins, le cerveau. »

      S’ensuit alors une recension de publications d’études statistiques (Royaume Uni et États-Unis) sur des cohortes de personnes Covid+, qui présentent toute une « palette » de symptômes qui ne disparaissent pas au bout de quelques semaines mais qui se prolongent durant des mois, voire bientôt deux ans. Ce qui, au final, ne paraît pas si incohérent puisque le système vasculaire irrigue le corps entier.

      Et on avait mis le doigt là-dessus depuis le début de la pandémie. Peut-on, sans trop passer pour de mauvais esprits, prétendre que les experts infectiologues et épidémiologistes autoproclamés ainsi que leur ministre Véran ont largement pédalé dans la semoule ? Voire nous ont pris carrément pour des buses ?
      je vous parle même pas de ceux qui ont prétendu que pour guérir du #Covid_long, il faut aller voir un psy.

  • COVID-19 isn’t just a cold

    This thread is long, and hard to read - not just because of the technical language, but because “it’s just a cold,” “the vaccine protects me,” and “at least our children are safe” are comforting fairy tales.

    I wish they were true.

    This virus is like measles and polio: a virus with long-term impact.

    Even a “mild” case in a vaccinated individual can lead to long-term issues which cause a measurable uptick in all-cause mortality in the first 6 months, and get progressively worse with time.

    SARS-CoV-2 is a systemic disease which has multiple avenues to induce long-term impairment, attacking the brain, heart, lungs, blood, testes, colon, liver, and lymph nodes, causing persistent symptoms in more than half of patients by six months out.

    The CoVHORT study, limited to non-hospitalized patients in Arizona - “mild” cases - found a 68% prevalence of 1 or more Covid symptom after 30 days, rising to 77% after 60 days. (We will explore an explanation later).

    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0254347

    To prevent panic, @CDCgov has been using the term “mild” to describe any case of COVID-19 which does not require hospitalization.

    #LongCOVID, however, is anything but “mild”, as the replies to @ahandvanish’s thread make heartbreakingly clear.

    https://twitter.com/ahandvanish/status/1423017721822949376

    A University of Washington study found that 30% of Covid patients had reduced Health Related Quality of Life, with 8% of the patients limited in routine daily activities.

    https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2776560

    These patients are struggling with real physical issues.

    This Yale study demonstrated reduced aerobic capacity, oxygen extraction. and ventilatory efficiency in “mild” COVID patients even after recovery from their acute infection.

    https://journal.chestnet.org/article/S0012-3692(21)03635-7/abstract

    It’s also a vascular disease. A Columbia study found “significantly altered lipid metabolism” during acute disease, which “suggests a significant impact of SARS-CoV-2 infection on red blood cell structural membrane homeostasis.”

    https://pubs.acs.org/doi/full/10.1021/acs.jproteome.0c00606

    Oregon Health & Science University found that “symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of [fatal] cardiovascular outcomes and has causal effect on all-cause mortality.”

    https://www.medrxiv.org/content/10.1101/2021.12.27.21268448v1

    Let’s review: SARS-CoV-2 causes an increase in mortality and reduced aerobic capacity even after asymptomatic cases, and remains in the body months after the initial infection.

    No, it’s not “just a cold.”

    But we’re just getting started. It gets worse. Way worse.

    The virus appears to be able to cross the blood-brain barrier and cause significant neurological damage.

    The ability of the spike protein to cross the blood-brain barrier was demonstrated in mice at the University of Washington.

    https://pubmed.ncbi.nlm.nih.gov/33328624

    A joint study by Stanford and Germany’s Saarland University found inflammation in the brain, and “show[ed] that peripheral T cells infiltrate the parenchyma.”

    https://www.nature.com/articles/s41586-021-03710-0

    For context, the parenchyma is the functional tissue of the brain - your neurons and glial cells. It isn’t normally where T cells are:

    “In the brain of healthy individuals, T cells are only present sporadically in the parenchyma.”

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6751344

    The Stanford study also discovered microglia and astrocytes which displayed “features .. that have previously been reported in human neurodegenerative disease.”

    Post-mortem neuropathology in Hamburg, Germany found “Infiltration by cytotoxic T lymphocytes .. in the brainstem and cerebellum, [with] meningeal cytotoxic T lymphocyte infiltration seen in 79% [of] patients.”

    https://www.sciencedirect.com/science/article/pii/S1474442220303082#

    An autopsy of a 14-month-old at Brazil’s Federal University of Rio de Janeiro found that “The brain exhibited severe atrophy and neuronal loss.”

    https://www.thelancet.com/journals/lanam/article/PIIS2667-193X(21)00038-7/abstract

    The UK Biobank COVID-19 re-imaging study compared before and after images of “mild” cases, and found “pronounced reduction in grey matter” and an “increase of diffusion indices, a marker of tissue damage” in specific regions of the brain.

    https://www.medrxiv.org/content/10.1101/2021.06.11.21258690v3

    That seems to explain why there is evidence of persistent cognitive deficits in people who have recovered from SARS-CoV2 infection in Great Britain.

    https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00324-2/fulltext

    Also worrisome are syncytia, where an infected cell extrudes its own spike protein and takes over its neighbors, fusing together to create a large multi-nucleus cell.

    Delta’s particular aptitude for this may partly explain its severity.

    https://www.news-medical.net/news/20211006/SARS-CoV-2-emerging-variants-display-enhanced-syncytia-formation.aspx

    And, yes, syncytia formation can happen in neurons. For our visual learners, here is video of syncytia and apoptosis (cell death) in a (bat) brain:

    https://twitter.com/nytimes/status/1429604323047133185

    Luckily, the University of Glasgow found that “Whilst Delta is optimised for fusion at the cell surface, Omicron .. achieves entry through endosomal fusion. This switch .. offers [an] explanation for [its] reduced syncytia formation.”

    https://www.gla.ac.uk/media/Media_829360_smxx.pdf

    If you’re interested in further understanding the host of neurological symptoms and the mechanisms underlying them, this Nature article is an excellent primer:

    https://www.nature.com/articles/d41586-021-01693-6

    Let’s review: SARS-CoV-2 can cross the blood-brain barrier, and even “mild” or asymptomatic cases can cause loss of neurons and persistent cognitive defects?

    That doesn’t sound “mild” to me; I like my brain.

    But it keeps getting worse.

    The brain isn’t the only organ affected: Testicular pathology has found evidence of “SARS-Cov-2 antigen in Leydig cells, Sertoli cells, spermatogonia, and fibroblasts” in post-morten examination.

    https://onlinelibrary.wiley.com/doi/10.1111/andr.13073

    A Duke pathology study in Singapore “detected SARS-CoV-2 .. in the colon, appendix, ileum, haemorrhoid, liver, gallbladder and lymph nodes .. suggesting widespread multiorgan involvement of the viral infection.”

    https://gut.bmj.com/content/gutjnl/early/2021/06/13/gutjnl-2021-324280.full.pdf#page1

    The same study found “evidence of residual virus in .. tissues during the convalescent phase, up to 6 months after recovery, in a non-postmortem setting,” suggesting that “a negative swab result might not necessarily indicate complete viral clearance from the body.”

    It also causes microclots: “Fibrin(ogen) amyloid microclots and platelet hyperactivation [were] observed in [Long COVID] patients,” in this work by Stellenbosch University of South Africa, which also explored potential treatments.

    https://www.researchsquare.com/article/rs-1205453/v1

    Let’s review - SARS-CoV2 attacks our veins, blood, heart, brain, testes, colon, appendix, liver, gallbladder and lymph nodes?

    No, it’s not “just a respiratory virus”.

    Not even close.

    There are also immunology implications:

    Johns Hopkins’ @fitterhappierAJ found that “CD95-mediated [T cell] differentiation and death may be advancing T cells to greater effector acquisition, fewer numbers, and immune dysregulation.”

    https://www.frontiersin.org/articles/10.3389/fimmu.2020.600405/full

    This Chinese military study of the initial Wuhan outbreak concluded that “T cell counts are reduced significantly in COVID-19 patients, and the surviving T cells appear functionally exhausted.”

    https://www.frontiersin.org/articles/10.3389/fimmu.2020.00827/full

    The study authors went on to warn, “Non-ICU patients with total T cells counts lower than 800/μL may still require urgent intervention, even in the immediate absence of more severe symptoms due to a high risk for further deterioration in condition.”

    Those warnings have since been proven by discovery of autoimmune features.

    This study of 177 Los Angeles healthcare workers found that all had persistent self-attacking antibodies at least 6 months after infection, regardless of illness severity.

    https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-03184-8

    In the words of T-cell immunologist Dr. Leonardi (@fitterhappierAJ)

    https://twitter.com/fitterhappierAJ/status/1475227891034210314

    This Kaiser Permanente S.California study found that, although natural immunity provided substantial protection against reinfection, “Hospitalization was more common at suspected reinfection (11.4%) than initial infection (5.4%).”

    https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(21)00422-5/abstract

    In fact, remember those cytokine storms? It turns out that even that even severe COVID-19 may not be a viral pneumonia, but an autoimmune attack of the lung.

    https://twitter.com/DaveLeeERMD/status/1413816137570205697

    Let’s review - it’s autoimmune: SARS-CoV2 convinces our body to attack itself.

    That might explain why the Arizona study saw more symptoms after 60 days than at 30 days.

    It also means “natural immunity” isn’t something to count on.

    But if you’re counting on vaccination to feel safe, there’s even more bad news.

    A study of Israel healthcare workers found that “Most breakthrough cases were mild or asymptomatic, although 19% had persistent symptoms (>6 weeks).”

    https://www.nejm.org/doi/full/10.1056/NEJMoa2109072

    Perhaps the most terrifying study is from Oxford University, which examined the effects of vaccination on long COVID symptoms, because not only did it find that vaccination does not protect against Long Covid, but that Long Covid symptoms become more likely over time:

    In the words of the study authors, “vaccination does not appear to be protective against .. long-COVID features, arrhythmia, joint pain, type 2 diabetes, liver disease, sleep disorders, and mood and anxiety disorders."

    https://www.medrxiv.org/content/10.1101/2021.10.26.21265508v3

    “The narrow confidence intervals rule out the possibility that these negative findings are merely a result of lack of statistical power. The inclusion of death in a composite endpoint with these outcomes rules out survivorship bias as an explanation.”

    That finding contradicts the findings from the UK Zoe app study, which found that “the odds of having symptoms for 28 days or more after post-vaccination infection were approximately halved by having two vaccine doses.”

    https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(21)00460-6/fulltext

    However, the structural limitations of the Zoe study - discussed in detail by @dgurdasani1 in the linked thread - may explain why it is particularly susceptible to bias against detecting a progressive degenerative condition.

    https://twitter.com/dgurdasani1/status/1422802883632893952

    Let’s review: we’ve now shown that vaccination appears to offer no protection against the long-term autoimmune effects of COVID - which we know causes T-cells to attack the lungs, and can cause T-cells to enter the brain.

    Why are we letting this run wild?!

    You may think, at least our children are safe.

    They are not.

    The CDC is tracking incidence of a life-threatening multisystem inflammatory syndrome in children following an acute COVID-19 infection, with 5,973 cases as of November 30, 2021.

    https://covid.cdc.gov/covid-data-tracker/#mis-national-surveillance

    Children also suffer from Long Covid.

    “More than half [of pediatric patients] reported at least one persisting symptom even 120 days [after] COVID-19, with 42.6% impaired by these symptoms during daily activities.”

    https://www.medrxiv.org/content/10.1101/2021.01.23.21250375v1

    Focusing exclusively on pediatric deaths is vastly underselling the danger to children.

    Anybody telling you that SARS-CoV-2 is “just a cold” or “safe for children” is lying to you. They are ignoring the massive body of research that indicates that it is anything but.

    Since our vaccines don’t stop transmission, and don’t appear to stop long-term illness, a “vaccination only” strategy is not going to be sufficient to prevent mass disability.

    This isn’t something we want to expose our kids to.

    Let’s review: even for children and vaccinated people, a “mild” case of COVID causes symptoms that point to long-term autoimmune issues, potentially causing our own body to attack our brains, hearts, and lungs.

    Scared? Good.

    Now we’re ready to get to work.

    “This is the virus most Americans don’t know. We were born into a world where a virus was a thing you got over in a few weeks.” — @sgeekfemale, to whom I owe a “thank you” for her editing assistance on this thread.

    The viruses they know in Kolkota, Kinshasa, and Wuhan are different: dangerous, lethal beasts.

    Since 2020, the field has been leveled. Willing or no, we’ve rejoined the rest of the world. We are, all of us, vulnerable in the face of an unfamiliar threat.

    The first step is acknowledging the threat.

    That means acknowledging that our response has been woefully inadequate, and that is going to be uncomfortable.

    The thought that we could have prevented this, but didn’t, will feel unconscionable to some.

    The knowledge that we could start preventing this today, but haven’t, is unconscionable to me.

    https://twitter.com/IanRicksecker/status/1426584062827712512

    It’s time to quit pretending “it’s just a cold,” or that there is some magical law of viruses that will make it evolve to an acceptable level.

    There’s no such law of evolution, just wishful thinking, easily disproven by:

    Ebola. Smallpox. Marburg. Polio. Malaria.

    There are things we can do to reduce our individual risk, immediately.

    That starts with wearing a good mask - an N95 or better - and choosing to avoid things like indoor dining and capacity-crowd stadiums.

    https://twitter.com/LazarusLong13/status/1440398111445188618

    This isn’t a choice of “individual freedom” vs “public health”. It isn’t “authoritarian” to ask people to change their behavior in order to save lives.

    https://www.thehastingscenter.org/individual-freedom-or-public-health-a-false-choice-in-the-covid-e

    As Arnold @Schwarzenegger argued so convincingly in @TheAtlantic, it is our patriotic duty:

    “Generations of Americans made incredible sacrifices, and we’re going to throw fits about putting a mask over our mouth and nose?”

    https://www.theatlantic.com/ideas/archive/2021/08/schwarzenegger-schmuck-mask-vaccines/619746

    “Those who would sacrifice essential liberty for a little bit of temporary security deserve neither!”

    What is the essential liberty here?

    It is the liberty to be able to breathe clean air, to live our lives without infecting our families and risking disability.

    To get there, we need to listen to our epidemiologists and public health experts - the ones who have been trying to tell us this since the beginning:

    https://twitter.com/EpiEllie/status/1444088804961304581

    It is time — long past time — to give up on the lazy fantasy that we can let it become “endemic” and “uncontrolled” because it inconveniences us, because it is killing our political opponents, or because the virus will magically evolve to some “mild” state.

    It is time — long past time — to begin controlling this virus.

    It’s possible: Japan, New Zealand, and South Korea have done it.

    It saves lives:

    It’s even good for the economy:

    “Globally, economic contraction and growth closely mirror increases and decreases in COVID-19 cases... Public health strategies that reduce SARS-CoV-2 transmission also safeguard the economy.”

    https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-021-06357-4

    It’s time.

    https://threadreaderapp.com/thread/1478611650760437765.html

    sur twitter :
    https://twitter.com/IanRicksecker/status/1478611650760437765

    #long-covid #covid-19 #coronavirus #covid_long #long_covid #séquelles #post-covid

  • Effectiveness of the first component of Gam-COVID-Vac (Sputnik V) on reduction of #SARS-CoV-2 confirmed infections, hospitalisations and mortality in patients aged 60-79: a retrospective cohort study in Argentina - EClinicalMedicine
    https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00406-5/abstract

    The study results indicate that in real life the first component of the Sputnik V vaccine confers high protection against laboratory-confirmed SARS-CoV-2 infections, COVID-19 hospitalisations and deaths in a population of 60-79 years of age.

    This effect was consistent in all subgroups tested.

    Our results could provide support for delaying the second dose in countries facing vaccine shortages to allow for higher population coverage with a single dose.

    Assessing the effectiveness of a single dose for a longer follow-up period than the 83 days tested in this study could be crucial to identifying the most appropriate length of time the second dose can be delayed.

    #vaccination #vaccins

  • Thread by chrischirp on Thread Reader App – Thread Reader App
    https://threadreaderapp.com/thread/1418696473177362432.html

    Prof. Christina Pagel sur Twitter : "#LONG_COVID THREAD:

    The people running the BBC Horizon “Great British Intelligence Test” challenge on over 80,000 people took the opportunity to see if they could detect any differences by whether people had had covid or not..." / Tw

    […]

    10. What if by the time there can be no doubt of long term problems in many people who’ve had covid, we’ve allowed millions more infections leaving hundreds of thousands more people affected.

    ONS estimated 634K people with long covid that impacts their life in June.

    11. For comparison, c. 260K people are diagnosed with diabetes & 500K with heart disease each year.

    I worry that we are creating a chronic disease tragedy right now.

    The Silent Pandemic - YouTube
    https://www.youtube.com/watch?v=3hplyClO1qw

  • Coronavirus : un peu moins de 6 patients sur 10 souffrent de problèmes neurologiques. Étude sur 841 patients hospitalisés à Albacete en Espagne

    6 de cada 10 pacientes con coronavirus desarrollaron algún problema neurológico
    https://www.elnacional.com/ciencia-tecnologia/6-de-cada-10-pacientes-con-coronavirus-desarrollaron-algun-problema-neur

    Un estudio publicado en la revista Neurology, el más extenso hasta la fecha, revisa a un total de 841 pacientes hospitalizados en Albacete, España, durante el mes de marzo

    Hasta 57,4% de los pacientes afectados por coronavirus ha desarrollado algún tipo de síntoma neurológico, según queda recogido en el trabajo llevado a cabo por un grupo de investigadores, liderado por el profesor de la Universidad de Castilla-La Mancha y jefe de Neurología del Hospital Universitario de Albacete, Tomás Segura.

    El trabajo, publicado en la revista Neurology, el más extenso hasta la fecha, revisa a un total de 841 pacientes hospitalizados en Albacete, España, durante el mes de marzo, informó en nota de prensa la universidad.

    Mialgias principalmente, además de cefaleas y encefalopatías son algunos de los síntomas neurológicos que han desarrollado hasta el 57,4% de los 841 pacientes que fueron hospitalizados en Albacete por covid-19 durante el mes de marzo, tal y como revela esta publicación de gran relevancia a nivel internacional, pues es uno de los primeros artículos que se publican sobre complicaciones neurológicas y sirve de base para sucesivas investigaciones y revisiones de la comunidad científica.

    • Neurologic manifestations in hospitalized patients with COVID-19: The ALBACOVID registry | Neurology
      https://n.neurology.org/content/early/2020/06/01/WNL.0000000000009937

      Abstract
      Objective: The coronavirus disease 2019 (COVID-19) has spread worldwide since December 2019. Neurological symptoms have been reported as part of the clinical spectrum of the disease. We aim to determine whether neurological manifestations are common in hospitalized COVID-19 patients and to describe their main characteristics.

      Methods: We systematically review all patients diagnosed with COVID-19 admitted to hospital in a Spanish population during March 2020. Demographic characteristics, systemic and neurological clinical manifestations, and complementary tests were analyzed.

      Results: Of 841 patients hospitalized with COVID-19 (mean age 66.4 years, 56.2% men) 57.4% developed some form of neurological symptom. Nonspecific symptoms such as myalgias (17.2%), headache (14.1%), and dizziness (6.1%) were present mostly in the early stages of infection. Anosmia (4.9%) and dysgeusia (6.2%) tended to occur early (60% as the first clinical manifestation) and were more frequent in less severe cases. Disorders of consciousness occurred commonly (19.6%), mostly in older patients and in severe and advanced COVID-19 stages. Myopathy (3.1%), dysautonomia (2.5%), cerebrovascular diseases (1.7%), seizures (0.7%), movement disorders (0.7%), encephalitis (n=1), Guillain-Barré syndrome (n=1), and optic neuritis (n=1) were also reported, but less frequent. Neurological complications were the main cause of death in 4.1% of all deceased study subjects.

      Conclusions: Neurological manifestations are common in hospitalized COVID-19 patients. In our series, more than half of patients presented some form of neurological symptom. Clinicians need to maintain close neurological surveillance for prompt recognition of these complications. The investigation of the mechanisms and emerging consequences of SARS-CoV-2 neurological involvement require further studies.

    • Il y a bien sûr une différence entre symptômes neurologiques et atteinte directe du système nerveux ; les symptômes par mécanisme indirect sont beaucoup plus fréquents : par exemple les insuffisances respiratoire, rénale, hépatique qui peuvent se voir dans toutes les infections graves et pas seulement dans la covid-19 se répercutent toutes sur le cerveau ; sans même aller jusque là une simple fièvre quelque soit son origine ou même une simple cystite sans fièvre peuvent entraîner une confusion mentale chez le sujet âgé.

    • emerging spectrum of COVID-19 neurology : clinical, radiological and laboratory findings | Brain | Oxford Academic
      https://academic.oup.com/brain/article/doi/10.1093/brain/awaa240/5868408

      Quand les symptômes neurologiques peuvent être regroupés en syndromes, les auteurs retiennent, de manière isolée ou associés, 5 mécanismes : les effets systémiques d’une infection grave (dans lesquels on peut compter les défaillances d’organes évoqués dans mon précédent post) le choc cytokinique et l’hyperinflammation (entre autres cérébrale) qui en résulte ; auto-immunité dite post infectieuse (dirigée contre le système nerveux central ou périphérique) ; atteinte vasculaire et/ou de la coagulation (responsable d’infarctus ou d’hémorragies cérébraux) ; une atteinte directe, mécanisme a priori exceptionnel.

      The potential mechanisms underpinning the syndromes described include either individually, or in combination, direct viral injury, a secondary hyperinflammation syndrome related to cytokines including IL-6 (Mehta et al., 2020), vasculopathy and/or coagulopathy, post-infectious inflammation including autoantibody production to neuronal antigens, and the effects of a severe systemic disorder with the neurological consequences of sepsis and hypoxia. Evidence of direct viral infection has proved elusive so far with only a few cases with SARS-CoV-2 in CSF reported, and few supportive histopathological features , though clearly further study would be helpful (Reichard et al., 2020, Von Weyhern et al., 2020). Elevation of pro-inflammatory cytokines was found to correlate with COVID-19 disease severity (Herold et al., 2020; Huang et al., 2020), and some patients responded to IL-1 or IL- 6 blockade (Cavalli et al., 2020; Price et al., 2020); in support of this possible mechanism, transient splenial lesions have been reported in a number of cases, including in children with multisystem inflammatory syndrome (MIS-C), in which elevated cytokines are thought to play a role (Starkey et al., 2017; Abdel-Mannan et al., 2020; Hayashi et al., 2020; Riollano- Cruz et al., 2020). Interestingly, some of the clinical features seen in our youngest patient (Patient 39, aged 16 with pseudotumour cerebri with cranial nerve palsies) overlapped with those seen in MIS-C, including gastrointestinal symptoms, rash and cardiac involvement (Supplementary Table 1). Exact mechanisms in each case will be largely speculative until clear clinical, radiological and histological correlates have been drawn; given the breadth of clinical presentations, it is likely that a number or spectrum of these mechanisms are involved.

    • Defining causality in #COVID-19 and neurological disorders | Journal of Neurology, Neurosurgery & Psychiatry
      https://jnnp.bmj.com/content/early/2020/06/04/jnnp-2020-323667

      Introduction

      Clinicians are increasingly recognising neurological presentations occur in some patients.1 A case series from Wuhan described associated neurological syndromes (eg, ‘dizziness’ and ‘impaired consciousness’), but with little detail regarding symptomatology, and cerebrospinal fluid (CSF) and neuroimaging findings.2 The extent to which these disorders were caused by the virus per se, rather than being complications of critical illness, unmasking of degenerative disease, or iatrogenic effects of repurposed medications is not clear.

      Numerous case reports have since emerged and, at the time of writing, published cases include encephalopathy,3 encephalitis,4 Guillain-Barré syndrome (GBS)5 and stroke.6 In most of these cases, the virus has been identified in respiratory samples, and in a small number in CSF. So far, the reporting of clinical features has been extremely variable, for example, several cases have claimed to report encephalitis without clear evidence of central nervous system (CNS) inflammation, which would not meet established definitions of the disease.7

      Whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is associated with neurological manifestations is of critical importance as this may result in substantial morbidity and mortality.

      Defining causality
      It is crucial that neurologists and neuropsychiatrists apply a systematic strategy to determine whether there is evidence that SARS-CoV2 is causing these manifestations, whether they are a consequence of severe systemic disease alone, or simply coincidence. In 1965, Hill proposed criteria on which to build an argument for disease causation, which can be applied to COVID-19.8

      What is the strength of the association?
      So far, it appears fairly weak . >2.5 million people have been infected with SARS-CoV2 and to date (to the authors’ knowledge) there have been only 93 published cases of neurological manifestations (about 5/100 000). However, reported cases are an underestimate of the real incidence, and this underscores the need for proper epidemiological study.

    • #Anosmie, #migraines… : ces symptômes neurologiques qui persistent #post-COVID
      https://francais.medscape.com/voirarticle/3606119

      Medscape édition française : Quels sont les troubles neurologiques que vous observez en post-Covid ?
      Pr Dominique Salmon–Ceron : Notre consultation post-Covid, où il y a beaucoup de passage, nous a permis de repérer un certain nombre de symptômes neurologiques persistants. Les patients rapportent notamment des sensations de fourmillements, de ruissellement qui touchent le plus souvent les membres mais qui peuvent aussi se situer autour du nez, de la tête ou ailleurs.
      Nous observons aussi des dysrégulations thermiques, des problèmes de déglutition, des migraines prolongées et des anosmies.
      Ces symptômes apparaissent quelque temps après la phase aiguë de l’infection alors que les patients vont mieux. Ils évoluent parfois par poussées successives. Mais, avec le temps, les poussées ont tendance à diminuer.

      Nous avons donc la preuve que le SARS-CoV-2 s’attaque au système nerveux ?
      Pr Salmon–Ceron : Le SARS-CoV-2 est clairement un virus avec un neurotropisme, une avidité pour le cerveau. Mais, nous ne savons pas trop ce qui se passe. Est-ce une réponse immune disproportionnée, la myéline est-elle atteinte ? Les études débutent. Pour l’instant nous n’avons pas de réponse.

      #covid-long

    • Maître Pandaï sur Twitter : "Étude de cohorte sur 60 patients, par IRM : « Nos résultats révèlent une possible perturbation de l’intégrité fonctionnelle du cerveau dans la phase de récupération du Covid-19, suggérant un potentiel de neuro-invasion de SARS-CoV-2. » https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(20)30228-5/fulltext" / Twitter
      https://twitter.com/Panda31808732/status/1292046348016066561

    • Neurological associations of COVID-19 - The Lancet Neurology
      https://seenthis.net/messages/872464

      Precise case definitions must be used to distinguish non-specific complications of severe disease (eg, hypoxic encephalopathy and critical care neuropathy) from those caused directly or indirectly by the virus, including infectious, para-infectious, and post-infectious encephalitis, hypercoagulable states leading to stroke, and acute neuropathies such as Guillain-Barré syndrome. Recognition of neurological disease associated with SARS-CoV-2 in patients whose respiratory infection is mild or asymptomatic might prove challenging, especially if the primary COVID-19 illness occurred weeks earlier. The proportion of infections leading to neurological disease will probably remain small . However, these patients might be left with severe neurological sequelae. With so many people infected, the overall number of neurological patients, and their associated health burden and social and economic costs might be large.