Shut and re-open: the role of schools in the spread of COVID-19 in Europe
AuthorsStage, Helena B.; orcid: 0000-0001-9938-8452; email: email@example.com
Shingleton, Joseph; orcid: 0000-0002-1628-3231; email: Joseph.Shingleton@phe.gov.uk
Ghosh, Sanmitra; orcid: 0000-0002-4879-7587
Scarabel, Francesca; orcid: 0000-0003-0250-4555
Pellis, Lorenzo; orcid: 0000-0002-3436-6487
Finnie, Thomas; orcid: 0000-0001-5962-4211
MetadataShow full item record
AbstractWe investigate the effect of school closure and subsequent reopening on the transmission of COVID-19, by considering Denmark, Norway, Sweden and German states as case studies. By comparing the growth rates in daily hospitalizations or confirmed cases under different interventions, we provide evidence that school closures contribute to a reduction in the growth rate approximately 7 days after implementation. Limited school attendance, such as older students sitting exams or the partial return of younger year groups, does not appear to significantly affect community transmission. In countries where community transmission is generally low, such as Denmark or Norway, a large-scale reopening of schools while controlling or suppressing the epidemic appears feasible. However, school reopening can contribute to statistically significant increases in the growth rate in countries like Germany, where community transmission is relatively high. In all regions, a combination of low classroom occupancy and robust test-and-trace measures were in place. Our findings underscore the need for a cautious evaluation of reopening strategies. This article is part of the theme issue ‘Modelling that shaped the early COVID-19 pandemic response in the UK’.
CitationPhilosophical Transactions of the Royal Society B, volume 376, issue 1829, page 20200277
PublisherThe Royal Society
DescriptionFrom The Royal Society via Jisc Publications Router
History: accepted 2020-12-02, pub-electronic 2021-05-31, pub-print 2021-07-19
Article version: VoR
Publication status: Published
Funder: Wellcome Trust; Id: http://dx.doi.org/10.13039/100004440; Grant(s): 202562/Z/16/Z
Funder: Royal Society; Id: http://dx.doi.org/10.13039/501100000288; Grant(s): 202562/Z/16/Z
Funder: Department for Health and Social Care
Funder: Canadian Institutes of Health Research; Id: http://dx.doi.org/10.13039/501100000024; Grant(s): 2019 Novel Coronavirus (COVID-19) rapid research
Funder: Medical Research Council; Id: http://dx.doi.org/10.13039/501100000265; Grant(s): MC UU 00002/11
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No Difference in Penetrance between Truncating and Missense/Aberrant Splicing Pathogenic Variants in MLH1 and MSH2: A Prospective Lynch Syndrome Database StudyDominguez-Valentin, Mev; orcid: 0000-0001-7856-0057; email: Mev.Dominguez.Valentin@rr-research.no; Plazzer, John-Paul; orcid: 0000-0001-5114-4301; email: firstname.lastname@example.org; Sampson, Julian R.; email: Sampson@cardiff.ac.uk; Engel, Christoph; orcid: 0000-0002-7247-282X; email: email@example.com; Aretz, Stefan; orcid: 0000-0002-5228-1890; email: firstname.lastname@example.org; Jenkins, Mark A.; email: email@example.com; Sunde, Lone; email: firstname.lastname@example.org; Bernstein, Inge; email: email@example.com; Capella, Gabriel; orcid: 0000-0002-4669-7320; email: firstname.lastname@example.org; Balaguer, Francesc; orcid: 0000-0002-0206-0539; email: email@example.com; et al. (MDPI, 2021-06-28)Background. Lynch syndrome is the most common genetic predisposition for hereditary cancer. Carriers of pathogenic changes in mismatch repair (MMR) genes have an increased risk of developing colorectal (CRC), endometrial, ovarian, urinary tract, prostate, and other cancers, depending on which gene is malfunctioning. In Lynch syndrome, differences in cancer incidence (penetrance) according to the gene involved have led to the stratification of cancer surveillance. By contrast, any differences in penetrance determined by the type of pathogenic variant remain unknown. Objective. To determine cumulative incidences of cancer in carriers of truncating and missense or aberrant splicing pathogenic variants of the MLH1 and MSH2 genes. Methods. Carriers of pathogenic variants of MLH1 (path_MLH1) and MSH2 (path_MSH2) genes filed in the Prospective Lynch Syndrome Database (PLSD) were categorized as truncating or missense/aberrant splicing according to the InSiGHT criteria for pathogenicity. Results. Among 5199 carriers, 1045 had missense or aberrant splicing variants, and 3930 had truncating variants. Prospective observation years for the two groups were 8205 and 34,141 years, respectively, after which there were no significant differences in incidences for cancer overall or for colorectal cancer or endometrial cancers separately. Conclusion. Truncating and missense or aberrant splicing pathogenic variants were associated with similar average cumulative incidences of cancer in carriers of path MLH1 and path_MSH2.
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