COVID–19, Journal de bord–18/02/2020–Questions a Francois Bricaire
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PROVIDER: S-EPMC7270777 | biostudies-literature | 2020 Mar
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC7204732 | biostudies-literature
Project description:Streptococcus agalactiae strain:18/19-02 | isolate:18/19-02 Genome sequencing
| PRJNA1006082 | ENA
Project description:Introdução Há evidências da associação da gravidade da COVID-19 com níveis séricos elevados da interleucina-18 (IL-18), as variantes genéticas desta citocina podem influenciar sua expressão e níveis séricos, contribuindo para a gravidade da COVID-19, há poucos estudos que correlacionam os polimorfismos genéticos da IL-18 com a gravidade desta doença, por isso buscamos contribuir para a compreensão da heterogeneidade clínica e desfecho em uma amostra da população brasileira de pacientes com COVID-19. Objetivo Avaliar a associação dos polimorfismos no gene da IL-18 com a gravidade clínica e desfecho da COVID-19 em uma amostra do estado do Paraná (PR). Método O estudo incluiu 158 pacientes de ambos os sexos, que recorreram ao serviço de atendimento hospitalar no período de junho a novembro de 2020 e que testaram positivo para SARS-CoV-2/RT-PCR+. Foram incluídos pacientes advindos da Universidade Estadual do Centro Oeste (UNICENTRO) de Guarapuava; da Universidade Estadual de Londrina (UEL) em Londrina e da Pontifícia Universidade Católica do Paraná (PUCPR) em Curitiba. As análises moleculares foram realizadas no Instituto para Pesquisa do Câncer (IPEC) de Guarapuava - PR. A coorte foi composta por 3 grupos e a estratificação dos casos foi feita por gravidade, conforme critérios estabelecidos pela Organização Mundial da Saúde. Resultados Avaliamos as variantes da IL-18 associados a gravidade da COVID-19 (casos leves x casos moderados e graves) e obtivemos os seguintes polimorfismos: rs360721 (alelos: C/G /freq: 0.22/ OR 1.603 (0.849; -3.026)/p: 0.1456), rs549908 (alelos: G/T /freq: 0.22/ OR 1.285 (0.6617; -2.496)/p: 0.4588), rs45497197 (alelos: T/C /freq: 0.01/ OR 0.2173 (0.01918; -2.463)/p: 0.2179), rs147751347 (alelos: T/G /freq: 0.02/ OR 1.532 (0.3591; -6.539)/p: 0.5643), rs141025779 (alelos: A/G / freq: 0.02/ OR 1.657 (0.3826; - 7.178)/ p: 0.4994), rs4988359 (alelos: C/T / freq: 0.14 / OR 1.166 (0.5261; -2.584)/p: 0.7052). Consideramos também a associação entre o desfecho clínico (recuperados x óbitos), neste cenário encontramos apenas uma variante: rs549908 (alelos: G/T / freq: 0.22 / OR 0.2556 (0.08; - 0.78)/p: 0.01757). Conclusão Esses achados sugerem que a variante do gene da IL-18, rs549908, está associado ao desfecho clínico da COVID-19 e que são necessários mais estudos para avaliar importância das variantes genéticas do gene da IL-18 como marcadores de prognóstico na doença. Ag. Financiadora Fundação Araucária.
| S-EPMC9461061 | biostudies-literature
Project description:COVID-19 has caused extensive human casualties with significant economic impacts around the globe, and has imposed new challenges on health systems worldwide. Over the past decade, SARS, Ebola, and Zika also led to significant concerns among the scientific community. Interestingly, the SARS and Zika epidemics ended before vaccine development; however, the scholarly community and the pharmaceutical companies responded very quickly at that time. Similarly, when the genetic sequence of SARSCoV-2 was revealed, global vaccine companies and scientists have stepped forward to develop a vaccine, triggering a race toward vaccine development that the whole world is relying on. Similarly, an effective and safe vaccine could play a pivotal role in eradicating COVID-19. However, few important questions regarding SARS-CoV-2 vaccine development are explored in this review.
| S-EPMC7771841 | biostudies-literature
Project description:Combinations of intense non-pharmaceutical interventions (lockdowns) were introduced worldwide to reduce SARS-CoV-2 transmission. Many governments have begun to implement exit strategies that relax restrictions while attempting to control the risk of a surge in cases. Mathematical modelling has played a central role in guiding interventions, but the challenge of designing optimal exit strategies in the face of ongoing transmission is unprecedented. Here, we report discussions from the Isaac Newton Institute 'Models for an exit strategy' workshop (11-15 May 2020). A diverse community of modellers who are providing evidence to governments worldwide were asked to identify the main questions that, if answered, would allow for more accurate predictions of the effects of different exit strategies. Based on these questions, we propose a roadmap to facilitate the development of reliable models to guide exit strategies. This roadmap requires a global collaborative effort from the scientific community and policymakers, and has three parts: (i) improve estimation of key epidemiological parameters; (ii) understand sources of heterogeneity in populations; and (iii) focus on requirements for data collection, particularly in low-to-middle-income countries. This will provide important information for planning exit strategies that balance socio-economic benefits with public health.
| S-EPMC7575516 | biostudies-literature
Project description:Résumé Contexte: La forme grave de COVID-19 semble affecter de manière disproportionnée les gens immunovulnérables, même si les données canadiennes dans ce contexte sont limitées. Nous avons voulu déterminer quels facteurs sont associés aux paramètres de la forme grave de COVID-19 chez les receveurs de transplantations au Canada. Méthodes: Nous avons procédé à une étude de cohorte multicentrique prospective regroupant tous les receveurs d’une transplantation d’organe plein ayant reçu un diagnostic de COVID-19 suivis dans 9 programmes de transplantation au Canada entre mars 2020 et novembre 2021. Les données ont été analysées afin de dégager les facteurs de risque à l’égard du recours à l’oxygénothérapie et autres critères de la gravité de la maladie. Nous avons comparé les paramètres selon le type d’organe transplanté et suivi l’évolution des paramètres au fil du temps. Nous avons procédé à une analyse multivariée pour déterminer quelles variables sont associées au recours à l’oxygénothérapie. Résultats: En tout, 509 patients ayant reçu une transplantation d’organe plein ont contracté la COVID-19 durant la période de l’étude. Les facteurs de risque associés au recours à l’oxygénothérapie (n = 190) ou non (n = 319) incluaient l’âge (âge médian 62,6 ans, intervalle interquartile [II] 52,5–69,5 ans c. âge médian 55,5 ans, II 47,5–66,5; p < 0,001) et le nombre de comorbidités (nombre médian 3, II 2–3 c. nombre médian 2, II 1–3; p < 0,001), de même que les paramètres concernant l’immunosuppression. Les receveurs d’une transplantation pulmonaire (n = 48) étaient plus susceptibles de souffrir d’une forme grave de la maladie, avec un taux de mortalité élevé (n = 15, 31,3 %) comparativement aux receveurs d’autres organes, y compris le rein (n = 48, 14,8 %), le cœur (n = 1, 4,4 %), le foie (n = 9, 11,4 %) et le rein–pancréas (n = 3, 12,0 %) (p = 0,02). Les facteurs protecteurs contre le recours à l’oxygénothérapie incluaient le fait d’avoir subi une transplantation hépatique et de recevoir de l’azathioprine. Le fait d’avoir reçu 2 doses de vaccin anti-SRAS-CoV-2 n’a pas eu d’influence appréciable sur le recours à l’oxygénothérapie. L’analyse multivariée a montré que l’âge avancé (rapport des cotes [RC] 1,04, intervalle de confiance [IC] de 95 % 1,02–1,07) et le nombre de comorbidités (RC 1,63, IC de 95 % 1,30–2,04), entre autres facteurs, étaient associés au recours à l’oxygénothérapie. La gravité de la maladie n’a pas considérablement diminué au fil du temps. Interprétation : Malgré les progrès thérapeutiques et la vaccination des receveurs d’une transplantation d’organe plein, les signes de gravité accrue de la COVID-19, en particulier chez les receveurs d’une transplantation pulmonaire, justifient le maintien des mesures de santé publique pour protéger ces personnes à risque, et l’utilisation hâtive de traitements contre la COVID-19 chez les receveurs d’une transplantation d’organe plein.
| S-EPMC9828967 | biostudies-literature
Project description:The spread of severe acute respiratory syndrome coronavirus 2 began later in Africa than in Asia and Europe. Senegal confirmed its first case of coronavirus disease on March 2, 2020. By March 4, a total of 4 cases had been confirmed, all in patients who traveled from Europe.
| S-EPMC7588548 | biostudies-literature
Project description: Not available
| S-EPMC8445275 | biostudies-literature
Project description:Vulnerability to coronavirus disease (COVID)-19 varies due to differences in interferon gamma (IFNγ) immunity. We investigated whether a key modifiable interferon precursor, interleukin-18, was related to COVID-19, overall and by severity, using Mendelian randomisation. We used four established genome-wide significant genetic predictors of interleukin-18 applied to the most recent genome-wide association study of COVID-19 (June 2021) to obtain Mendelian randomisation inverse variance weighted estimates by severity, i.e. any (cases = 112 612, non-cases = 2 474 079), hospitalised (cases = 24 274, non-cases = 2 061 529) and very severe (cases = 8779, non-cases = 1 001 875) COVID-19. To be comprehensive, we also conducted an exploratory analysis for IFNγ and two related cytokines with less well-established genetic predictors, i.e. interleukin-12 and interleukin-23. Genetically predicted interleukin-18 was associated with lower risk of any COVID-19 (odds ratio (OR) 0.96 per standard deviation, 95% confidence interval (0.94-0.99, P-value 0.004)) and of very severe COVID-19 (OR 0.88, 95% CI 0.78-0.999, P-value 0.048). Sensitivity analysis and a more liberal genetic instrument selection gave largely similar results. Few genome-wide significant genetic predictors were available for IFNγ, interleukin-12 or interleukin-23, and no associations with COVID-19 were evident. Interleukin-18 could be a modifiable target to prevent COVID-19 and should be further explored in an experimental design.
| S-EPMC8755530 | biostudies-literature
Project description:Policies and measures to control pandemics are often failing. While biological factors controlling transmission are usually well explored, little is known about the environmental drivers of transmission and infection. For instance, respiratory droplets and aerosol particles are crucial vectors for the airborne transmission of the severe acute respiratory syndrome coronavirus 2, the causation agent of the coronavirus 2019 pandemic (COVID-19). Once expectorated, respiratory droplets interact with atmospheric particulates that influence the viability and transmission of the novel coronavirus, yet there is little knowledge on this process or its consequences on virus transmission and infection. Here we review the effects of atmospheric particulate properties, vortex zones, and air pollution on virus survivability and transmission. We found that particle size, chemical constituents, electrostatic charges, and the moisture content of airborne particles can have notable effects on virus transmission, with higher survival generally associated with larger particles, yet some viruses are better preserved on small particles. Some chemical constituents and surface-adsorbed chemical species may damage peptide bonds in viral proteins and impair virus stability. Electrostatic charges and water content of atmospheric particulates may affect the adherence of virion particles and possibly their viability. In addition, vortex zones and human thermal plumes are major environmental factors altering the aerodynamics of buoyant particles in air, which can strongly influence the transport of airborne particles and the transmission of associated viruses. Insights into these factors may provide explanations for the widely observed positive correlations between COVID-19 infection and mortality with air pollution, of which particulate matter is a common constituent that may have a central role in the airborne transmission of the novel coronavirus.Supplementary informationThe online version contains supplementary material available at 10.1007/s10311-022-01557-z.
| S-EPMC9816530 | biostudies-literature