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  • États-Unis : une intelligence artificielle est parvenue à prédire des crimes avec 90% d’efficacité

    Des chercheurs de l’Université de Chicago ont créé une intelligence artificielle capable de prédire les lieux et dates de crimes dans plusieurs villes américaines. Elle a atteint un taux de succès de 90%, d’après les auteurs.


    On va leur demander de tester leur modèle sur les tueries de masse dans les établissements scolaires.

  • Face masks for COVID pass their largest test yet

    Critics of mask mandates have cited the lack of relevant randomized clinical trials, which assign participants at random to either a control group or an intervention group. But the latest finding is based on a randomized trial involving nearly 350,000 people across rural Bangladesh. The study’s authors found that surgical masks — but not cloth masks — reduced transmission of #SARS-CoV-2 in villages where the research team distributed face masks and promoted their use.

    #masques #covid-19

  • Why call it BA.2.12.1? A guide to the tangled Omicron family

    Given all these #variants, is #SARS-CoV-2 evolving more rapidly than other viruses?

    Not necessarily, Rambaut says. Researchers are finding an incredible amount of diversity in SARS-CoV-2, but they’re also sequencing this virus at an unprecedented rate. A record 11 million SARS-CoV-2 genomes have been uploaded to the popular GISAID data platform since January 2020. By contrast, researchers have uploaded about 1.6 million sequences of the influenza virus to GISAID’s EpiFlu database since May 2008.

    Still, Rambaut says, many questions remain about how SARS-CoV-2 is evolving, because sequencing is nearly absent in some parts of the world, and some countries with raging outbreaks are scaling back genomic surveillance.

    Could Omicron’s subvariants, such as BA.4, eventually receive Greek names?

    Yes, although it hasn’t happened yet. Some researchers argue that the Omicron subvariants currently fuelling surges, such as BA.4 and BA.2.12.1, deserve simpler names to aid communication with governments and the public at a time when regard for COVID-19 control measures, such as face masks, is waning. They also point out that unlike Delta’s subvariants — which were not discussed much in the media — BA.4 and BA.2.12.1 can overcome immunity provided by earlier infections with other Omicron subvariants. This was unexpected, says Houriiyah Tegally, a bioinformatician at the Centre for Epidemic Response and Innovation in Stellenbosch, South Africa. “ Everyone thought that only new variants would cause new waves, but now that we’re seeing that Omicron can do it, maybe we should adapt the system of naming ,” she suggests.

    But the WHO is so far resisting this idea. WHO virologist Lorenzo Subissi says that the capacity for immune evasion isn’t wildly different between Omicron subvariants. He adds that the agency’s assessment could change if future studies prove that an Omicron subvariant causes more severe disease than other Omicron varieties. The technical lead of the WHO’s COVID-19 response, Maria Van Kerkhove, adds that the agency also doesn’t recommend swapping a technical label for a Greek name in the hope of spurring leaders to take the ongoing pandemic more seriously. “This is already a scary virus, it is still killing huge numbers of people unnecessarily,” she says, suggesting that world leaders should already be paying attention.

  • COVID and smell loss: answers begin to emerge | Nature | 09.06.22

    Columbia University in New York City examined people who had died from COVID-19 and found that, although their neurons were intact, they had fewer membrane-embedded receptors for detecting odour molecules than usual. This was because the neurons’ nuclei had been scrambled. Normally, the chromosomes in these nuclei are organized into two compartments — a structure that enables the neurons to express specific odour receptors at high levels. But when the team looked at the autopsied neurons, “the nuclear architecture was unrecognizable,” Lomvardas says.

    Other studies suggest why only some people experience long-term smell loss. In January, a research team reported finding a genetic mutation in people that was associated with a greater propensity for smell or taste loss. The mutation — a change to a single ‘letter’, or base, of DNA — was found in two overlapping genes, called UGT2A1 and UGT2A2. Both encode proteins that remove odour molecules from the nostrils after they have been detected. But it’s not yet clear how SARS-CoV-2 interacts with these genes.

    There is also evidence of lasting changes to the brain for people with smell loss. [...] “When we cut off input from the nose, the brain atrophies,” says Danielle Reed, a geneticist also at Monell. “It’s one of the clearest things we know about taste and smell.”

  • Le réchauffement climatique accélère le cycle de l’#eau

    Quelles conséquences pour la Planète ? Dans un monde qui se réchauffe à plus 2 °C, le cycle de l’eau va s’accélérer de 4 à 8 %. Et les régions déjà sèches vont devenir encore plus sèches. Avec des conséquences sur le bétail et les cultures et une augmentation du risque d’incendies de forêt. À l’inverse, d’autres régions connaîtront des pluies plus fortes. Les précipitations associées aux cyclones et aux ouragans continueront d’augmenter, causant plus de dommages encore.

    Source :
    Observed poleward freshwater transport since 1970 | Nature


  • Monkeypox goes global : why scientists are on alert

    More than 120 confirmed or suspected cases of monkeypox, a rare viral disease seldom detected outside of Africa, have been reported in at least 11 non-African countries in the past week. The emergence of the virus in separate populations across the world where it doesn’t usually appear has alarmed scientists — and sent them racing for answers.

    Synthèse de l’article en français :


  • #Bacteriophage treatment of disseminated cutaneous Mycobacterium chelonae infection | Nature Communications

    We report a case of refractory cutaneous disseminated M. chelonae infection in a patient with seronegative arthritis on immunotherapy with tofacitinib that was treated with combination antimicrobial, surgical, and single bacteriophage therapy with excellent clinical response. The patient developed neutralizing antibodies against the bacteriophage but continues to have stable improvement of disease with negative biopsies and no evidence of bacterial resistance to the phage.


    Bacteriophage therapy using a cocktail of multiple phage isolates has been recently successfully used for the treatment of resistant bacterial infections including multidrug-resistant nontuberculous mycobacterial infections in conjunction with traditional antibiotic therapy. Widespread use of bacteriophage therapy is limited by logistic and regulatory challenges as well as the development of bacterial resistance or neutralizing antibodies that may reduce host response to the bacteriophage.


    To our knowledge, this is the first case of a human M. chelonae infection treated with a bacteriophage, and the first case of bacteriophage treatment with a single phage for a mycobacterial infection. Bacteriophage therapy is a promising therapeutic option for multi-drug resistant infections, though improved understanding of safety, the factors driving the development of bacterial resistance, and the clinical significance of antibody-mediated phage neutralization is vital to advance this therapeutic option for patients.

  • Le virus mangeur de cerveau | Nature | oct. 2021

    The SARS-CoV-2 main protease Mpro causes microvascular brain pathology by cleaving NEMO in brain endothelial cells


    Coronavirus disease 2019 (COVID-19) can damage cerebral small vessels and cause neurological symptoms. Here we describe structural changes in cerebral small vessels of patients with COVID-19 and elucidate potential mechanisms underlying the vascular pathology. In brains of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected individuals and animal models, we found an increased number of empty basement membrane tubes, so-called string vessels representing remnants of lost capillaries. We obtained evidence that brain endothelial cells are infected and that the main protease of SARS-CoV-2 (Mpro) cleaves NEMO, the essential modulator of nuclear factor-κB. By ablating NEMO, Mpro induces the death of human brain endothelial cells and the occurrence of string vessels in mice. Deletion of receptor-interacting protein kinase (RIPK) 3, a mediator of regulated cell death, blocks the vessel rarefaction and disruption of the blood–brain barrier due to NEMO ablation. Importantly, a pharmacological inhibitor of RIPK signaling prevented the Mpro-induced microvascular pathology. Our data suggest RIPK as a potential therapeutic target to treat the neuropathology of COVID-19.

    • Des preuves d’invasion cérébrale | JEM | janvier 2021

      Neuroinvasion of SARS-CoV-2 in human and mouse brain

      Although COVID-19 is considered to be primarily a respiratory disease, SARS-CoV-2 affects multiple organ systems including the central nervous system (CNS). Yet, there is no consensus on the consequences of CNS infections. Here, we used three independent approaches to probe the capacity of SARS-CoV-2 to infect the brain. First, using human brain organoids, we observed clear evidence of infection with accompanying metabolic changes in infected and neighboring neurons. However, no evidence for type I interferon responses was detected. We demonstrate that neuronal infection can be prevented by blocking ACE2 with antibodies or by administering cerebrospinal fluid from a COVID-19 patient. Second, using mice overexpressing human ACE2, we demonstrate SARS-CoV-2 neuroinvasion in vivo. Finally, in autopsies from patients who died of COVID-19, we detect SARS-CoV-2 in cortical neurons and note pathological features associated with infection with minimal immune cell infiltrates. These results provide evidence for the neuroinvasive capacity of SARS-CoV-2 and an unexpected consequence of direct infection of neurons by SARS-CoV-2.

      via @Dowser

  • Le changement climatique favorise la transmission des #virus entre les #espèces, selon une étude

    Pour survivre face au changement climatique dans leur région respective, certaines espèces vont devoir se déplacer et parcourir des centaines de kilomètres vers d’autres territoires. Elles vont emporter avec elles leurs parasites et agents pathogènes. Le changement climatique va ainsi pousser les espèces à se mélanger et à créer des rencontres jusque-là inédites, alors qu’elles évoluaient chacune dans des environnements séparés. Cela va favoriser les risques de transmission de virus et d’autres bactéries potentiellement dangereuses.

    Mais cette nouvelle coexistence d’espèces qui va devenir plus large ne se limitera pas à la seule transmission virale entre animaux. Les scientifiques assurent que ces échanges viraux risquent de provoquer des #zoonoses, des transmissions de virus des animaux aux humains. « Nous avons l’habitude de penser que le risque est plus élevé dans les pays tropicaux, car ils ont plus de biodiversité, des plateformes d’échanges plus risquées comme les marchés d’animaux sauvages, mais ce changement monumental qui intervient dans les écosystèmes fait du risque pandémique le problème de tout le monde », précise Colin Carlson, qui a coécrit l’étude.

    Source :
    Climate change increases cross-species viral transmission risk | Nature

    At least 10,000 virus species have the capacity to infect humans, but at present, the vast majority are circulating silently in wild mammals1,2.


  • Nouveau volet de l’étude sur le Covid long

    [TAC | lun. 18 avr. 2022 | 18:20]

    Le projet de recherche ComPaRe, conjointement mené par l’AP-HP et Université de Paris, dévoile un autre volet de son étude sur les formes longues du Covid-19.

    De nouveaux travaux au sein de la cohorte ComPaRe Covid long ont révélé que 85 % des patients qui avaient eu des symptômes persistants rapportaient encore des symptômes de Covid-19 douze mois après le début de la maladie. Un an après le début des symptômes, 60 % des patients déplorent un impact très important de la maladie sur leur vie personnelle, professionnelle et sociale.

    À l’occasion de cette publication, ComPaRe lance un nouvel appel à la participation à l’ensemble des patients souffrant de Covid long. ComPaRe, la communauté de patients pour la recherche, rassemble aujourd’hui plus de 50 000 volontaires. Pour participer, appuyez sur le lien ci-dessous.

    (unable to open URL :-) goOgLe is your friend)

  • Accelerated biological aging in COVID-19 patients | Nature Communications

    En fait, quand un #covid_long te dit qu’il vit comme dans le corps d’un gus de 80 ans, ce n’est pas tout à fait qu’un ressenti… 👀

    Chronological age is a risk factor for SARS-CoV-2 infection and severe COVID-19. Previous findings indicate that epigenetic age could be altered in viral infection. However, the epigenetic aging in COVID-19 has not been well studied. In this study, DNA methylation of the blood samples from 232 healthy individuals and 413 COVID-19 patients is profiled using EPIC methylation array. Epigenetic ages of each individual are determined by applying epigenetic clocks and telomere length estimator to the methylation profile of the individual. Epigenetic age acceleration is calculated and compared between groups. We observe strong correlations between the epigenetic clocks and individual’s chronological age (r > 0.8, p < 0.0001). We also find the increasing acceleration of epigenetic aging and telomere attrition in the sequential blood samples from healthy individuals and infected patients developing non-severe and severe COVID-19. In addition, the longitudinal DNA methylation profiling analysis find that the accumulation of epigenetic aging from COVID-19 syndrome could be partly reversed at late clinic phases in some patients. In conclusion, accelerated epigenetic aging is associated with the risk of SARS-CoV-2 infection and developing severe COVID-19. In addition, the accumulation of epigenetic aging from COVID-19 may contribute to the post-COVID-19 syndrome among survivors.

    • Tu es sûr·e que c’est covid long et pas covid sous forme grave ? Autrement dit ceux qui sont en réa mais n’en sortent pas les pieds devant
      A moins que ce ne soit systématique que l’un implique l’autre (je ne crois pas) ?

    • Ce qu’on sait depuis deux ans maintenant, mais qu’on a du mal à admettre, comme pour l’aérosolisation, c’est que c’est aléatoire, et ça concerne tous les contaminés. Les formes légères comme graves peuvent passer dans le corps sans laisser de séquelles. Tout comme l’exact opposé. Le truc à retenir, c’est que le virus peut abimer des vaisseaux sanguins partout, et que partout, donc, des organes vont pouvoir dysfonctionner plus ou moins gravement et plus ou moins longtemps. Avec les conséquences diverses qu’on connait. Comme les épidémies de bidules qui touchent le foie des enfants, et qu’on croit que c’est un nouveau virus mais qu’en fait c’est documenté depuis des mois que ce type d’effets secondaires existent suite à un covid, même léger (cf. les informations d’hier à ce sujet largement diffusées sur les canaux généralistes qui ont oublié de vérifier si par hasard, ce n’était pas évident que c’était une suite du covid).

    • Vacciné ou pas ? Il y a des covid longs de personnes vaccinées, oui. Mais pas d’idées claires de probas, je ne suis pas allé voir ce que ça dit récemment. Je retiens qu’il vaut mieux être vacciné, et qu’il vaut mieux ne pas l’avoir du tout. Comme pour l’assurance incendie de ton logement.


      vers minute 7 :

      la vaccination semble réduire les chiffres des covid longs

      et, minute 6 :

      avoir été hospitalisé [cas « grave »] ou pas [cas « léger » voire asympto] ne change pas radicalement le nb de symptômes rapportés

      ceci dit, minute 10 :

      hospitalistrion / cas grave = risque très accru de conséquences à long terme


      les non hospitalisés ont très peu voire pas de différence [nb de pb rapportés] avec le groupe contrôle « saints », sauf pour les myocardites

      et à 10:38 (une question sur la vax)

      la vax comme traitement pour les gens qui ont un covid longs [...] [pour régler un éventuel pb de persistance virale] résultat : un tout petit peu efficace [...] pre-print de septembre 2021

  • Même les #cactus redoutent le réchauffement climatique -

    […] selon une étude menée par des chercheurs de l’université de l’Arizona qui remet en question l’hypothèse selon laquelle ces plantes prospéreront avec la hausse des températures.

    Source :
    Elevated extinction risk of cacti under climate change | Nature Plants


  • Persistent COVID-19 symptoms in a community study of 606,434 people in England | Nature Communications

    Table 1 shows the proportion of people with COVID-19 who still reported one or more, or three or more, of 29 symptoms at 12 weeks after symptom onset. At 12 weeks, 37.7% (37.4,38.1) of those in rounds 3–5 reported one or more symptoms, and 17.5% (17.2,17.7) reported three or more; in round 6, these figures were 21.6% (20.9,22.3) and 11.9% (11.4,12.5), respectively. For rounds 3–5, these translated to a weighted population prevalence of 5.80% (5.73,5.86) for having, or having had, one or more persistent symptoms for 12 weeks or more, and 2.23% (2.19,2.27) for three or more persistent symptoms. In round 6 the equivalent percentages were 3.06% (2.98,3.14) and 1.61 (1.56,1.67), respectively, for 27 symptoms in common with rounds 3–5 (Supplementary Table 5), increasing to 3.26% (3.18,3.34) and 1.86% (1.80,1.92) for one and three symptoms respectively if all 35 symptoms surveyed in round 6 are included (Supplementary Table 6).

  • Neuropathology and virus in brain of SARS-CoV-2 infected non-human primates | Nature Communications

    Neurological manifestations are a significant complication of coronavirus disease (COVID-19), but underlying mechanisms aren’t well understood. The development of animal models that recapitulate the neuropathological findings of autopsied brain tissue from patients who died from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are critical for elucidating the neuropathogenesis of infection and disease. Here, we show neuroinflammation, microhemorrhages, brain hypoxia, and neuropathology that is consistent with hypoxic-ischemic injury in SARS-CoV-2 infected non-human primates (NHPs), including evidence of neuron degeneration and apoptosis. Importantly, this is seen among infected animals that do not develop severe respiratory disease, which may provide insight into neurological symptoms associated with “long COVID”. Sparse virus is detected in brain endothelial cells but does not associate with the severity of central nervous system (CNS) injury. We anticipate our findings will advance our current understanding of the neuropathogenesis of SARS-CoV-2 infection and demonstrate SARS-CoV-2 infected NHPs are a highly relevant animal model for investigating COVID-19 neuropathogenesis among human subjects.

    Signalé par Maître Pandaï avec un extrait traduit :

    « Ici, nous montrons une neuroinflammation, des micro-hémorragies, une hypoxie du cerveau et une neuropathologie cohérente avec des lésions hypoxiques-ischémiques chez les primates non-humains infectés par SARS-CoV-2, avec des preuves de dégénérescence et d’apoptose des neurones. De façon importante, ces phénomènes sont observés chez les animaux infectés qui ne développent pas de maladie respiratoire sévère, ce qui pourrait fournir des connaissances sur les symptômes neurologiques associés au Covid long »

    « Nos résultats de lésions hypoxiques-ischémiques dans le cerveau des primates non-humains sont en phase avec les autopsies du cerveau chez des sujets humains. »

    « Même des réductions mineures, mais durables de l’[apport en] oxygène pourraient favoriser des lésions, particulièrement parmi les neurones, qui semblent avoir souffert le plus dans cette étude »

    « Les lésions neuronales ne semblaient pas être la conséquence directe d’une infection du virus (...). À la place, les lésions et morts neuronales se produisaient très probablement par manque d’énergie, ce qui est une conséquence première des évènements hypoxiques-ischémiques. »

    « Il est raisonnable d’anticiper que des résultats similaires pourraient se produire chez les sujets humains, particulièrement ceux avec des symptômes neurologiques persistants après l’infection »

    Hé ben ça donne encore plus envie de l’attraper, ce simple rhume.

  • Morgue data hint at COVID’s true toll in Africa

    Around 90% of deceased people tested at a Lusaka facility during coronavirus surges were positive for #SARS-CoV-2 infection, suggesting flaws in the idea of an ‘African paradox’.

    Trying to Solve a Covid Mystery: Africa’s Low Death Rates - The New York Times

    But many scientists tracking the pandemic on the ground disagree. It’s not possible that hundreds of thousands or even millions of Covid deaths could have gone unnoticed, they say.

    “We have not seen massive burials in Africa. If that had happened, we’d have seen it,” said Dr. Thierno Baldé, who runs the W.H.O.’s Covid emergency response in Africa.

    “A death in Africa never goes unrecorded, as much as we are poor at record-keeping,” said Dr. Abdhalah Ziraba, an epidemiologist at the African Population and Health Research Center in Nairobi, Kenya. “There is a funeral, an announcement: A burial is never done within a week because it is a big event. For someone sitting in New York hypothesizing that they were unrecorded — well, we may not have the accurate numbers, but the perception is palpable. In the media, in your social circle, you know if there are deaths.”

    Dr. Demby, the Sierra Leone health minister, who is an epidemiologist by training, agreed. “We haven’t had overflowing hospitals. We haven’t,” he said. “There is no evidence that excess deaths are occurring.”

    Which could be keeping the death rate lower?

    #mortalité #covid-19 #Afrique

  • Evaluation of science advice during the COVID-19 pandemic in Sweden | Humanities and Social Sciences Communications

    We argue that that scientific methodology was not followed by the major figures in the acting authorities—or the responsible politicians—with alternative narratives being considered as valid, resulting in arbitrary policy decisions. In 2014, the Public Health Agency merged with the Institute for Infectious Disease Control; the first decision by its new head (Johan Carlson) was to dismiss and move the authority’s six professors to Karolinska Institute. With this setup, the authority lacked expertise and could disregard scientific facts. (…)

    Many elderly people were administered morphine instead of oxygen despite available supplies, effectively ending their lives.

    If Sweden wants to do better in future pandemics, the scientific method must be re-established, not least within the Public Health Agency. It would likely make a large difference if a separate, independent Institute for Infectious Disease Control is recreated. We recommend Sweden begins a self-critical process about its political culture and the lack of accountability of decision-makers to avoid future failures, as occurred with the COVID-19 pandemic.

    #in_retrospect #suède

  • Antigenic evolution will lead to new #SARS-CoV-2 #variants with unpredictable severity | Nature Reviews Microbiology

    The comparatively milder infections with the Omicron variant and higher levels of population immunity have raised hopes for a weakening of the pandemic. We argue that the lower severity of Omicron is a coincidence and that ongoing rapid antigenic evolution is likely to produce new variants that may escape immunity and be more severe.

  • Sci-Hub downloads show countries where pirate paper site is most used

    Sci-Hub downloads show countries where #pirate_paper_site is most used

    La France se classe juste derrière la Chine et les Etats-Unis dans un classement international significatif : le nombre de téléchargements sur le site russe Sci-Hub :

    Le nombre de #téléchargements témoigne de l’emprise des #éditeurs privés sur leur #clientèle_captive, qui se trouve être aussi celle qui produit leur richesse : nous. Si l’on rapporte le nombre de téléchargements sur Sci-Hub au nombre de chercheurs, la #France est encore 4ème, derrière la Colombie, les Philippines et la Malaisie, et juste avant l’Indonésie et le Brésil. Il y a 7 fois plus d’articles téléchargés par chercheur en France qu’en Allemagne…
    Cet engouement pour Sci-Hub témoigne évidemment du caractère dysfonctionnel des #bibliothèques_numériques_françaises, surtout pour les accès à distance. L’association #Couperin, en charge de la contractualisation avec les éditeurs, négocie un accès différencié pour les différents établissements et, à l’intérieur de ceux-ci, pour les différentes disciplines. Toute recherche multidisciplinaire se transforme ainsi en cauchemar… sauf à utiliser #Sci-Hub.

    via #Rogue :