• #Airborne transmission of respiratory viruses | Science

    The COVID-19 pandemic has revealed critical knowledge gaps in our understanding of and a need to update the traditional view of transmission pathways for respiratory viruses. The long-standing definitions of droplet and airborne transmission do not account for the mechanisms by which virus-laden respiratory droplets and aerosols travel through the air and lead to infection. In this Review, we discuss current evidence regarding the transmission of respiratory viruses by aerosols—how they are generated, transported, and deposited, as well as the factors affecting the relative contributions of droplet-spray deposition versus aerosol inhalation as modes of transmission. Improved understanding of aerosol transmission brought about by studies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection requires a reevaluation of the major transmission pathways for other respiratory viruses, which will allow better-informed controls to reduce airborne transmission.

  • Airborne transmission of respiratory viruses | Science

    Phases involved in airborne transmission of respiratory viruses.
    Virus-laden aerosols (<100 I1/4m) are first generated by an infected individual through expiratory activities, through which they are exhaled and transported in the environment. They may be inhaled by a potential host to initiate a new infection, provided that they remain infectious. In contrast to droplets (>100 I1/4m), #aerosols can linger in air for hours and travel beyond 1 to 2 m from the infected individual who exhales them, causing new infections at both short and long ranges.

  • Durability of mRNA-1273 vaccine–induced antibodies against #SARS-CoV-2 #variants | Science

    SARS-CoV-2 #mutations may diminish vaccine-induced protective immune responses, particularly as antibody titers wane over time. Here, we assess the impact of SARS-CoV-2 variants B.1.1.7 (Alpha), B.1.351 (Beta), P.1 (Gamma), B.1.429 (Epsilon), B.1.526 (Iota), and B.1.617.2 (Delta) on binding, neutralizing, and ACE2-competing antibodies elicited by the vaccine mRNA-1273 over seven months. Cross-reactive neutralizing responses were rare after a single dose. At the peak of response to the second vaccine dose, all individuals had responses to all variants. Binding and functional antibodies against variants persisted in most subjects, albeit at low levels, for 6-months after the primary series of the mRNA-1273 vaccine. Across all assays, B.1.351 had the lowest antibody recognition. These data complement ongoing studies to inform the potential need for additional boost vaccinations.

    #immunité #vaccins #vaccination

  • Scent of a vaccine | Science

    À propos de la #vaccination par voie nasale

    Compared to intramuscular vaccines, intranasal vaccines provide two additional layers of protection: Vaccine-elicited IgA and resident memory B and T cells in the respiratory mucosa provide an effective barrier to infection at those sites; and, even if infection does occur, perhaps by a viral variant, cross-reactive, resident memory B and T cells, which encounter antigen earlier and respond more quickly than systemic memory cells, impede viral replication and reduce viral shedding and transmission (see the figure).

    Routes of vaccination
    Immunoglobulin A (IgA) and resident memory B and T cells in the nasal passages and upper airways are elicited by intranasal vaccination and prevent infection and reduce virus shedding. Serum IgG elicited by intramuscular vaccination transudates into the lungs and prevents pulmonary infection but allows infection in the nasal passages and virus shedding.


  • Origine du Sars-Cov2 : la vérité s’est-elle échappée du laboratoire ?

    La revue scientifique Science publie ce 13 mai 2021 une lettre d’une vingtaine de chercheurs américains, réclamant une enquête sur les origines du Sars-Cov-2. « Nous devons considérer sérieusement les deux hypothèses, celle de l’origine animale et celle de la fuite d’un laboratoire jusqu’à ce que nous ayons suffisamment de données », écrivent-ils. De son côté, le rédacteur en chef explique : « Le but de notre rubrique Science’s Insights est d’offrir aux scientifiques le meilleur espace de discussion sur la science. Aussi, vu l’importance du sujet, l’ampleur de l’expertise et les qualifications éminentes des auteurs, la décision de publier leur lettre était facile. » Quel intéressant moment. Il n’est pas donné tous les jours d’assister à d’aussi impudents retournements de vestes, à en attraper des (...)

    http://www.piecesetmaindoeuvre.com/spip.php?page=resume&id_article=1469 #Nécrotechnologies

  • Unreliable social science research gets more attention than solid studies

    In 2011, a striking psychology paper made a splash across social media, news, and academia: People used the internet as a form of “external” memory (https://science.sciencemag.org/content/333/6040/277), the study said, relying on it for information rather than recalling facts themselves. In 2018, a key finding from that paper failed to replicate when a team of psychologists put it and 20 other high-profile social science studies (https://www.sciencemag.org/news/2018/08/generous-approach-replication-confirms-many-high-profile-social-science-) to the test.

    But the original paper has been cited 1417 times—with more than 400 of those citations coming after the 2018 replication project. That’s far more, on average, than the papers from the project that did replicate. Now, a new study shores up the popularity of unreliable studies: Social science papers that failed to replicate racked up 153 more citations, on average, than papers that replicated successfully.

    This latest result is “pretty damning,” says University of Maryland, College Park, cognitive scientist Michael Dougherty, who was not involved with the research. “Citation counts have long been treated as a proxy for research quality,” he says, so the finding that less reliable research is cited more points to a “fundamental problem” with how such work is evaluated.

    University of California, San Diego, economists Marta Serra-Garcia and Uri Gneezy were interested in whether catchy research ideas would get more attention than mundane ones, even if they were less likely to be true. So they gathered data on 80 papers from three different projects that had tried to replicate important social science findings, with varying levels of success.

    Citation counts on Google Scholar were significantly higher for the papers that failed to replicate, they report today in Science Advances, with an average boost of 16 extra citations per year. That’s a big number, Serra-Garcia and Gneezy say—papers in high-impact journals in the same time period amassed a total of about 40 citations per year on average.

    And when the researchers examined citations in papers published after the landmark replication projects, they found that the papers rarely acknowledged the failure to replicate, mentioning it only 12% of the time.

    A failed replication doesn’t necessarily mean the original finding was false, Serra-Garcia points out. Changes in methods and evolving habits among participants—like changing patterns of internet use—may explain why an old result might not hold up. But she adds that her findings point to a fundamental tension in research: Scientists want their work to be accurate, but they also want to publish results that are attention grabbing. It might be that peer reviewers lower their bar for evidence when the results are particularly surprising or exciting, she says, which could mean striking results and weaker evidence often go hand in hand.

    The guideline that “extraordinary claims require extraordinary evidence” seems to soften when it comes to publication decisions, agrees Massey University computational biologist Thomas Pfeiffer, who studies replication issues, but was not involved with this work. That points to the need for extra safeguards to bolster the credibility of published work, he says—like a higher threshold for what counts as good evidence, and more effort to focus on strong research questions and methods, rather than flashy findings.

    “The finding is catnip for [research] culture change advocates like me,” says Brian Nosek, a psychologist at the University of Virginia who has spearheaded a number of replication efforts and was a co-author on two of the three replication projects that Serra-Garcia and Gneezy drew from. But before taking it too seriously, it’s worth seeing whether this finding itself can be replicated using different samples of papers, he says.

    The result falls in line with previous studies that suggest popular research is less reliable. A 2011 study in Infection and Immunity, for example, found that high-impact journals have higher retraction rates than lower impact ones (https://journals.asm.org/doi/full/10.1128/IAI.05661-11). And Dougherty’s research—currently an unreviewed preprint—has found that more highly cited papers were based on weaker data, he says. But a 2020 paper in the Proceedings of the National Academy of Sciences that looked at a different sample of papers found no relationship between citation and replication. That suggests the sample of papers could really matter, Pfeiffer says—for instance, the effect could be particularly strong in high-impact journals.

    Nosek adds that stronger but less sensational papers may still accrue more citations over the long haul, if the popularity contest of striking results burns out: “We’ve all seen enough teen movies to know that the popular kid loses in the end to the brainy geek. Maybe scientific findings operate in the same way: Credible ones don’t get noticed as much, but they do persist and win in the end.”

    #recherche #sciences_sociales #citations #qualité #impact #science #popularité #rétraction

  • A New #Coronavirus May Be Making People Sick. And It’s Coming From Dogs : Goats and Soda : NPR

    Zhang has studied coronaviruses for more than 30 years. He thinks it’s too early to call this new virus a human pathogen. “As the authors are careful to say in their paper, they have not proven what’s called Koch’s postulates,” he says. That is, Vlasova, Gray and colleagues haven’t shown that the new coronavirus causes pneumonia; so far, it has only been associated with the disease.

    “To do that, strictly, they need to inject the virus into humans and see if it reproduces the disease,” he says. “Of course [for ethical reasons], we cannot do that.”

    Instead, Zhang says, they can look to see how common the virus is in pneumonia patients around the world — and they can test to see whether it makes mice or another animal sick.


  • Our immune systems blanket the #SARS-CoV-2 spike protein with antibodies | EurekAlert! Science News

    Previous research focused on one group of antibodies that target the most obvious part of the coronavirus’s spike protein, called the receptor-binding domain (RBD). Because the RBD is the part of the spike that attaches directly to human cells and enables the virus to infect them, it was rightly assumed to be a primary target of the immune system. But, testing blood plasma samples from four people who recovered from SARS-CoV-2 infections, the researchers found that most of the antibodies circulating in the blood — on average, about 84% — target areas of the viral spike protein outside the RBD — and, apparently, for good reason.

    “We found these antibodies are painting the entire spike, both the arc and the stalk of the spike protein, which looks a bit like an umbrella,” [...] “The immune system sees the entire spike and tries to neutralize it.”

    Many of these non-RBD-directed antibodies the team identified act as a potent weapon against the virus by targeting a region in a part of the spike protein located in what would be the umbrella’s canopy called the N-terminal domain (NTD). These antibodies neutralize the virus in cell cultures and were shown to prevent a lethal mouse-adapted version of the virus from infecting mice.

    The NTD is also a part of the viral spike protein that mutates frequently, especially in several variants of concern. This suggests that one reason these #variants are so effective at evading our immune systems is that they can mutate around one of the most common and potent types of antibody in our arsenals.


    Despite these maneuvers by SARS-CoV-2, the researchers said about 40% of the circulating antibodies target the stalk of the spike protein, called the S2 subunit, which is also a part that the virus does not seem able to change easily.

    “That’s reassuring,” Ippolito said. “That’s an advantage our immune system has. It also means our current vaccines are eliciting antibodies targeting that S2 subunit, which are likely providing another layer of protection against the virus.”


    Source: Prevalent, protective, and convergent IgG recognition of SARS-CoV-2 non-RBD spike epitopes | Science

  • #COVID-19 : Le #variant brésilien capable d’échappement immunitaire | santé log

    Sur la base d’un modèle épidémiologique pour estimer son degré de transmissibilité, les chercheurs estiment que P.1 est susceptible d’être entre 1,7 et 2,4 fois plus transmissible que les lignées non-P1 du coronavirus.

    Enfin, ils concluent également que P.1 est susceptible de pouvoir échapper à entre 10 et 46% de l’#immunité acquise par une infection par un coronavirus non-P.1.
    Des résultats qui appellent à une surveillance accrue des infections et des différentes souches du virus absolument indispensable pour parvenir à maîtriser la pandémie.

    Source :
    Genomics and epidemiology of the P.1 #SARS-CoV-2 lineage in #Manaus, Brazil | Science

  • #SARS-CoV-2 #transmission without symptoms | Science

    Viral replication and symptom onset
    The titer of infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the amount of viral RNA are generally lower in asymptomatic (A) than presymptomatic (Pre) #COVID-19. There is likely to be a threshold at which a person becomes contagious, but this is not known. In presymptomatic patients, symptoms usually begin when viral load peaks, so there is a period of infectiousness when a person has no symptoms.

    #asymptomatiques #pré-symptomatiques #contagiosité

  • Immunity to #SARS-CoV-2 #variants of concern | Science

    Vaccine-induced protection
    Loss of neutralizing epitopes in the spike protein in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants could reduce protection induced by vaccination based on wild-type spike. Most vaccinated people develop neutralizing antibody (Ab) with an IC50 (half maximal inhibitory concentration) within the protective margin, although precise correlates of protection (CoP) are unknown. Variants with E484K mutations and future escape mutants may bring protection below this margin, prompting the need for new vaccines.

    #vaccination #vaccins #vaccin

    • Référence 4 de la bibliographie de l’article :

      Efficacy of ChAdOx1 nCoV-19 (AZD1222) vaccine against SARS-CoV-2 VOC 202012/01 (B.1.1.7)

      Malgré une activité neutralisante divisée par 9 vis-à-vis du variant « britannique », le vaccin Oxford/AstraZeneca est aussi efficace contre ce dernier qu’il l’est vis-à-vis du virus « chinois ».

      Virus neutralisation activity by vaccine- induced antibodies was 9-fold lower against the B.1.1.7 variant than against a canonical non- B.1.1.7 lineage.

      Vaccine efficacy against symptomatic NAAT positive infection was similar for B.1.1.7 and non-B1.1.7 lineages (74.6% [95%CI 41.6-88.9] and 84% [95% CI 70.7-91.4] respectively). [...]

      Efficacy of ChAdOx1 nCoV-19 against the B.1.1.7 variant of SARS-CoV-2 is similar to the efficacy of the vaccine against other lineages. Furthermore, vaccination with ChAdOx1 nCoV-19 results in a reduction in the duration of shedding and viral load, which may translate into a material impact on transmission of disease.

    • De l’article de Science :

      It has been posited that SARS-CoV-2 may continue to accumulate mutations that evade immune responses (10). But as previously explored for other viruses, such as HIV, immune evasion often comes at a biological fitness cost to the virus , tending to impose an upper limit to the number of mutations that can be afforded when faced with a broad, neutralizing antibody repertoire (11).

  • Prospective mapping of viral mutations that escape antibodies used to treat COVID-19 | Science

    Of course, our maps still do not answer the most pressing question: will SARS-CoV-2 evolve widespread resistance to these antibodies? But certainly, it is concerning that so many escape mutations impose little cost on RBD folding or receptor affinity, and that some are already present at low levels among circulating viruses. Ultimately, it will be necessary to wait and see what mutations spread as #SARS-CoV-2 circulates in the human population. Our work will help with the “seeing,” by enabling immediate interpretation of the effects of the mutations cataloged by viral genomic surveillance.

    #variants #vaccins

  • Est-ce que, vu que ça fait un an que ça dure, on a une théorie un peu sérieuse sur l’effet de l’arrivée de l’été sur le virus ?

    Parce que de ce que je vois, la situation est mauvaise en ce moment au Brésil, où c’est l’été.

    Je vous dis ce que je crains ? Si on continue avec ces pseudo-confinements qui se contentent de bloquer la progression, sans réellement d’effet à la baisse, on va se maintenir à des niveaux très élevés de circulation du virus, et je ne vois pas dans ce cas comment on pourrait rouvrir quoi que ce soit de restauration, de bistrots et de culturel pour l’été.

    À moins que le pari est que d’ici là, on aura vacciné au moins la population la plus fragile, et que donc on pourra laisser s’ébattre le virus dans la population, avec un taux de mortalité bien plus faible et donc sans saturer les réas. Ce qui me semble un choix excessivement risqué.

    • L’immunité de troupeau naturelle à partir d’une vague initiale n’existe pas (#Manaus). Les seuls « vaccins » (in)disponibles ont des effets dont on ne sait pas à quel point ils sont limités. Le pari : compter sur des mutations nombreuses pour obtenir une immunité de troupeau naturelle, à moyen terme....

      Immunological characteristics govern the transition of COVID-19 to endemicity - View ORCID ProfileJennie S. Lavine1,*, View ORCID ProfileOttar N. Bjornstad2, View ORCID ProfileRustom Antia1

      We are currently faced with the question of how the CoV-2 severity may change in the years ahead. Our analysis of immunological and epidemiological data on endemic human coronaviruses (HCoVs) shows that infection-blocking immunity wanes rapidly, but disease-reducing immunity is long-lived. Our model, incorporating these components of immunity, recapitulates both the current severity of CoV-2 and the benign nature of HCoVs, suggesting that once the endemic phase is reached and primary exposure is in childhood, CoV-2 may be no more virulent than the common cold. We predict a different outcome for an emergent coronavirus that causes severe disease in children. These results reinforce the importance of behavioral containment during pandemic vaccine rollout, while prompting us to evaluate scenarios for continuing vaccination in the endemic phase.


    • Ah, Christian Drosten aborde très exactement ces deux points (effet de l’été, laisser filer l’épidémie une fois les personnes fragiles vaccinées) dans son interview de la semaine :

      Drosten: Once the elderly and maybe part of the risk groups have been vaccinated, there will be immense economic, social, political and perhaps also legal pressure to end the corona measures. And then, huge numbers of people will become infected within just a short amount of time, more than we can even imagine at the moment. We won’t have 20,000 or 30,000 new cases a day, but up to 100,000 in a worst-case scenario. It will, of course, be primarily younger people who are less likely than older people to have severe symptoms, but when a huge number of younger people get infected, then the intensive care units will fill up anyway and a lot of people will die. Just that it will be younger people. We can cushion this terrible scenario somewhat by pushing the numbers way down now.

      DER SPIEGEL: Can we be confident that case numbers will begin to drop in spring as temperatures rise?

      Drosten: I don’t think so. The fact that we had such a relaxed summer in 2020 likely had to do with the fact that our case numbers remained below a critical threshold in the spring. But that’s not the case any longer. I am afraid that it will be more like in Spain, where case numbers climbed rapidly again after the lockdown was lifted, even though it was quite hot. In South Africa, too, where it is currently summer, case numbers are at a high level.

  • Fallen giant | Science

    The story of the collapse of the #Arecibo telescope is now well known. On 10 August 2020, a steel cable supporting a 900-ton instrument platform high above the dish broke at one end and fell, slicing into the dish. A second support cable snapped on 6 November and the National Science Foundation said attempting repairs was too dangerous: Arecibo would be dismantled. On 1 December, fate took control as more cables snapped and the platform came crashing down into the dish. The loss dismayed scientists worldwide. Although 57 years old, Arecibo was still a scientific trailblazer. The public, familiar with the majestic dish from films such as Contact and GoldenEye, also felt the loss. And it was a bitter blow to the people of Puerto Rico, who embraced hosting the technological marvel. Some experts think manufacturing flaws or poor maintenance doomed the suspension cables. Others blame dwindling funding levels. But astronomers are looking to the future. Last month, researchers announced plans for a new $400 million telescope on the same site.

  • Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection | Science

    #COVID-19 : De bonnes nouvelles sur le front de l’immunité | santé log

    L’équipe de Jennifer M Dan du Center for Infectious Disease and Vaccine Research du La Jolla Institute for Immunology (Californie) a donc recruté plus de 180 hommes et femmes rétablis du COVID-19. 7% de ces participants avaient été hospitalisés mais la majorité avait développé une forme légère de la maladie. La plupart des participants ont fourni un échantillon de sang dès le 6è à 8è jour après l’apparition des symptômes. Les chercheurs ont pu suivre ainsi dans 254 échantillons au total, provenant de 188 cas de COVID-19, les anticorps, les cellules B (qui produisent les anticorps) et deux types de cellules T (qui tuent les cellules infectées). Ce suivi montre que :
    les anticorps, dont les anticorps dirigés contre les composants de la protéine de pointe, ne présentent que des baisses modestes 6 à 8 mois après l’apparition des symptômes ; les cellules T, ne montrent qu’une légère « décomposition » au fil du temps, les cellules B ont augmenté en nombre dans certains cas.

    Protective immunity against #SARS-CoV-2 could last eight months or more | EurekAlert! Science News

    The team cautions that protective immunity does vary dramatically from person to person. In fact, the researchers saw a 100-fold range in the magnitude of immune memory. People with a weak immune memory may be vulnerable to a case of recurrent COVID-19 in the future, or they may be more likely to infect others.

    “There are some people that are way down at the bottom of how much immune memory they have, and maybe those people are a lot more susceptible to reinfection,” says Crotty.

    #immunité #anticorps

  • Autour du vin -Vins et Santé- : Des composés du raisin bloquent une enzyme clé du virus de la covid-19

    D’après des chercheurs américains, les flavanols et proanthocyanidines du raisin et du vin empêchent le virus du SRAS-CoV-2 de se fixer sur les cellules humaines. Ces polyphénols également présents dans le thé vert et le cacao pourraient ainsi aider à lutter contre la pandémie.
    On connaissait les propriétés antivirales de certains fruits comme le kaki. Des chercheurs de l’Université de Caroline du Nord viennent de constater que des extraits bruts de thé vert, de cacao, et deux variétés de la famille des muscadines (Vitis rotundifolia) récoltées aux Etats-Unis comme raisin de table ou de cuve sont également capables de freiner l’activité du SRAS-Cov-2 à l’origine de la Covid-19.

    « Ces aliments abondants en flavan-3-ols et en proanthocyanidines perturbent la manière dont le virus se réplique et se fixe aux cellules humaines » indique De-Yu Xie, l’auteur principal de l’étude. 

    "Expériences in vitro "
    Les chercheurs ont réalisé des expériences in vitro en laboratoire pour découvrir que ces polyphénols compliquaient la vie du virus en se liant à sa protéase Mpro et assurent qu’ils auraient toute leur place dans une thérapie contre la pandémie.
    En avril, une équipe chinoise avait synthétisé deux composés inhibiteurs de l’enzyme Mpro, avec de bons résultats in vivo sur le chien et la souris. Ils avaient publié leurs travaux dans la revue Science. https://science.sciencemag.org/content/368/6497/1331.full

  • Afucosylated IgG characterizes enveloped viral responses and correlates with COVID-19 severity | Science

    IgG antibodies are crucial for protection against invading pathogens. A highly conserved N-linked glycan within the IgG-Fc tail, essential for IgG function, shows variable composition in humans. Afucosylated IgG variants are already used in anti-cancer therapeutic antibodies for their elevated activity through Fc receptors (FcγRIIIa). Here, we report that afucosylated IgG (~6% of total IgG in humans) are specifically formed against enveloped viruses but generally not against other antigens. This mediates stronger FcγRIIIa responses, but also amplifies brewing cytokine storms and immune-mediated pathologies. Critically ill COVID-19 patients, but not those with mild symptoms, had high levels of afucosylated IgG antibodies against SARS-CoV-2, amplifying pro-inflammatory cytokine release and acute phase responses. Thus, antibody glycosylation plays a critical role in immune responses to enveloped viruses, including COVID-19.

  • Eurosurveillance | Secondary transmission of COVID-19 in preschool and school settings in northern Italy after their reopening in September 2020: a population-based study

    Schools in Reggio Emilia province, northern Italy, reopened on 1 September 2020 after a long period of closure due to lockdown and summer holidays. We conducted epidemiological investigations after reopening in 41 classes in 36 different educational settings in this province after the notification of an infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

    The first wave of the coronavirus disease (COVID-19) pandemic hit the Reggio Emilia province (northern Italy, 530,000 inhabitants) in March and April 2020, reaching ca 0.9% cumulative incidence (0.4% for age < 50 years and 3.2% for age > 80 years) with a more than 15% fatality rate (0.2% for age < 50 years and 33.4% for age > 80 years) [1,2]. After 5 months of low incidence, the province began the second wave in October (Figure).

    Figure. Daily number of notified COVID-19 cases and deaths since the start of the epidemic in Italy, Reggio Emilia province, 27 February–10 November 2020 (n = 11,878 cases, n = 658 deaths)

    Graphique parlant que l’ajout du suffixe #.jpeg (qui fonctionne fort bien pour toutes sortes d’image non reconnues par seenthis) ne permet pas de faire apparaître ici :


    Transmission within the schools of Reggio Emilia province, northern Italy, occurred in a non-negligible number of cases, particularly in the age group 10–18 years, i.e. in middle and high schools, while no secondary cases were detected in pre-school children, only one case in primary school and no secondary cases among teachers and staff. At least in the largest cluster that we reported, more prompt isolation and testing of classmates could have reduced virus transmission, suggesting the importance of timeliness in this setting.

    #covid-19 #école #enfants

    • Lockdown light, écoles, demi-classes, réduction des contacts, #vaccin et fin de pandémie. Podcast #68 du 8 décembre 2020 [partie 1], une traduction du podcast de Christian Drosten

      (...) l’impression domine que la situation scolaire est sérieuse. Vous pouvez voir qu’il y a une incidence considérable dans les écoles. On doit simplement le reconnaître. [...] Nous avons de bonnes données d’Angleterre qui donnent un aperçu et qui disent que ce sont surtout dans les années après l’école primaire qu’il y a plus d’infections que dans la population normale. L’étude REACT-1 https://www.gov.uk/government/publications/react-1-study-of-coronavirus-transmission-october-2020-interim-results/react-1-real-time-assessment-of-community-transmission-of-coronavirus-covid-19-i, par exemple, le montre très clairement. Nous n’avons pas d’étude comparable en Allemagne. Mais il n’y a aucune raison de penser que ce serait différent ici qu’en Angleterre.

      Il existe une étude intéressante menée par deux institutions de sciences sociales, l’Université Columbia et l’Université de Mannheim. [Social network-based strategies for classroom size reduction can help limit outbreaks of SARS-CoV-2 in high schools. A simulation study in classrooms of four European countries https://www.medrxiv.org/content/10.1101/2020.11.30.20241166v1] (...) Les écoles sont des nœuds importants. Un cas à l’école est plus important pour la transmission dans la population qu’un cas dans d’autres groupes d’âge.

      [...] les écoles sont impliquées dans la grippe, mais c’est aussi un événement endémique. Et avec une infection pandémique, on s’attend à ce que si les écoles sont touchées, elles seront probablement plus importantes en proportion pour propager la maladie à la population. Je pense que c’est encore important dans la deuxième vague. Il faut clarifier cela à nouveau.

      Il existe une étude de simulation intéressante de ce groupe de travail qui traite précisément de cela. Que peut-on convenablement évaluer et recommander [pour] les écoles. Ils ont utilisé un ensemble de données empiriques très intéressant. À savoir les données des années précédentes, bien avant la pandémie. Des enquêtes sur les comportements de contact ont été réalisées dans les écoles d’Europe, notamment en Angleterre, en Allemagne, aux Pays-Bas et en Suède. Le tout était centré sur la neuvième année, les 14 à 15 ans.

      [...] À un moment donné, il faudra ouvrir complètement. [...] La population se compose non seulement de patients à haut risque, mais aussi de l’économie et chacun doit faire valoir ses droits. Les événements ne seront plus empêchés ou le nombre de participants réduit. Bien entendu, les prochaines élections générales joueront également un rôle dans toutes ces tensions. Nous arriverons à un moment où les infections dans la population seront généralisées. Nous n’aurons jamais vu cela auparavant. En été, nous aurons alors un effet température qui nous profitera tout comme il l’a fait l’été dernier avec, remarquez, des mesures existantes. Nous sortirons alors de l’été et verrons également un grand nombre d’infections dans une population que nous n’avions pas encore. Dans la population en bonne santé, normale et plus jeune où il n’y a pas de facteurs de risque. Les enfants, par exemple, seront alors fortement infectés, tout comme leurs parents. Même les jeunes adultes qui ne présentent aucun facteur de risque. Nous verrons ensuite un autre type de patient dans les unités de soins intensifs en Allemagne. À savoir ceux qui, en pleine santé, ont développé de manière inattendue une forme sévère. Nous les voyons déjà maintenant, ils sont parfois déjà là. Ils seront alors en grand nombre. Et d’ici là, nous devrons certainement avoir quelque chose de prêt pour ces patients. À savoir de meilleures approches pharmaceutiques pour le traitement de la maladie grave chez ces patients sans risque.

      Bien entendu, la vaccination active se poursuivra alors et le processus de contaminations s’arrêtera de plus en plus, par une combinaison entre ceux qui ont été infectés et ceux qui ont été vaccinés. Mais pour ceux qui seront bêtement frappés, les préparations d’anticorps devront être mises à disposition, c’est-à-dire des mélanges d’anticorps monoclonaux, qui auront très certainement été approuvés. [...] On peut espérer que les prix seront complètement différents lorsque des quantités plus importantes seront demandées. Il faudra également progresser avec l’immunothérapie. Donc avec les substances. Ce ne sont parfois pas des anticorps bon marché qui peuvent influencer l’évolution inflammatoire sévère de la maladie dans la phase de traitement intensif. Ce qui, tout simplement, sauve les poumons. La recherche doit à nouveau s’intensifier. Ensuite, toute la chaîne de rapports politiques jusqu’au ministère de la Santé doit à nouveau s’en occuper. Les prochains problèmes sont déjà préprogrammés. On n’en parle pas encore en public, mais c’est clair pour moi. Je vais le dire ici maintenant, nous ne débarrasserons pas rapidement la population du risque au printemps en vaccinant les groupes à risque, puis en déclarant la pandémie terminée.

    • Fêtes de fin d’année : rater l’école pour mieux lutter contre le Covid

      Dans une note publiée lundi soir, le #Conseil_scientifique recommande de ne pas pénaliser les absences scolaires des 17 et 18 décembre pour permettre aux enfants de se confiner avant Noël

      ... que faire des enfants scolarisés, eux, jusqu’au 18 décembre ? Pour le Conseil scientifique, la seule solution, c’est que l’Education nationale fasse preuve d’un peu de souplesse. Il faudrait « laisser une tolérance aux familles qui le peuvent et qui le souhaitent d’élargir de deux jours la période des vacances scolaires afin que l’autoconfinement d’une semaine soit également possible pour les enfants »

      Au Pays des Lumières éteintes, l’article ne relève aucun autre problème que celui que cela va poser aux parents....


    • En début de semaine, le Groupe JP Vernant avait retouité un message avec la recommandation d’au minimum fermer les cantines cette semaine.

      Quand j’ai lu ça, la première chose que j’ai pensé, c’est : « Ah ben évidemment que non ils vont pas le faire : ce serait admettre qu’on se contamine dans les cantines… ».

      Sinon, puisqu’on en est désormais à admettre que les gamins se contaminent à l’école puis contaminent leurs familles, ça pose un nouveau souci pour Blanquer : s’il y a (comme assez largement prévu) un redémarrage de l’épidémie dans les prochaines semaines, qu’est-ce qu’on fait pour la rentrée scolaire ? On refait mine que les enfants ne contaminent personne et on reconfine tout le monde sauf les écoles ? On prétend qu’on a installé des purificateurs d’air invisibles dans toutes les classes pendant les vacances ?

    • Inferring the effectiveness of government interventions against COVID-19

      Governments are attempting to control the COVID-19 pandemic with nonpharmaceutical interventions (NPIs). However, the effectiveness of different NPIs at reducing transmission is poorly understood. We gathered chronological data on the implementation of NPIs for several European, and other, countries between January and the end of May 2020. We estimate the effectiveness of NPIs, ranging from limiting gathering sizes, business closures, and closure of educational institutions to stay-at-home orders . To do so, we used a Bayesian hierarchical model that links NPI implementation dates to national case and death counts and supported the results with extensive empirical validation. Closing all educational institutions, limiting gatherings to 10 people or less, and closing face-to-face businesses each reduced transmission considerably. The additional effect of stay-at-home orders was comparatively small.

      #confinement #mesures_sanitaires

    • Nouvelle méthode de détermination de la prévalence en Angleterre : de l’école au lycée, contamination massive : REACT-1 round 7 updated report : regional heterogeneity in changes in prevalence of SARS-CoV-2 infection during the second national COVID-19 lockdown in England



  • Three-quarters attack rate of SARS-CoV-2 in the Brazilian Amazon during a largely unmitigated epidemic | Science

    our data show that >70% of the population has been infected in Manaus approximately seven months after the virus first arrived in the city. This is above the theoretical herd immunity threshold. However, prior infection may not confer long-lasting immunity (…). Manaus represents a “sentinel” population, giving us a data-based indication of what may happen if SARS-CoV-2 is allowed to spread largely unmitigated.

  • Encore rares, les #réinfections nous donnent des indices sur le fonctionnement de l’#immunité

    Pour qu’une réinfection soit avérée, le patient doit avoir effectué deux tests PCR (réaction en chaîne par polymérase) positifs, sans avoir présenté de symptôme pendant au moins un mois entre les deux. Chantal Reusken, virologue à l’Institut néerlandais de la santé publique et de l’environnement (RIVM), précise toutefois qu’un deuxième test peut également être positif soit parce que le patient a gardé dans les voies respiratoires des résidus d’ARN viral non réplicatif issus de la primo-infection, soit parce qu’il avait jugulé le virus sans jamais véritablement l’éliminer.

    C’est pourquoi, explique Paul Moss, hématologue à l’université de Birmingham, la plupart des revues médicales veulent voir entre la première et la deuxième infection deux séquences virales à part entière, très différentes l’une de l’autre. “La barre est très haute, dit-il. Dans bien des cas, il n’y a même pas la moindre trace de matériel génétique [du virus].”

    Et même si cet ARN est présent, de nombreux laboratoires n’ont ni assez de temps ni assez d’argent pour le détecter. De ce fait, le nombre de réinfections attestées par des séquences génétiques reste très inférieur au nombre de suspicions de réinfection.


    Reinfections, still rare, provide clues on immunity | Science