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Critical Care Medicine ; 50:81-81, 2022.
Article in English | Academic Search Complete | ID: covidwho-1595844


B Introduction: b Previous work has shown correlations of zinc deficiency and poor outcomes in COVID-19 patients.i Little is known, however, about the use of zinc supplementation and its potential benefits in hospitalized COVID-19 positive individuals. B Conclusions: b Zinc use may be associated with improved clinical outcomes in hospitalized COVID-19 patients. [Extracted from the article] Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

medrxiv; 2021.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2021.05.22.21257633


Despite regional successes in controlling the SARS-CoV-2 pandemic, global cases have reached an all time high in April 2021 in part due to the evolution of more transmissible variants. Here we use the dense genomic surveillance generated by the COVID-19 Genomics UK Consortium to reconstruct the dynamics of 62 different lineages in each of 315 English local authorities between September 2020 and April 2021. This analysis reveals a series of sub-epidemics that peaked in the early autumn of 2020, followed by a singular jump in transmissibility of the B.1.1.7 lineage. B.1.1.7 grew when other lineages declined during the second national lockdown and regionally tiered restrictions between November and December 2020. A third more stringent national lockdown eventually suppressed B.1.1.7 and eliminated nearly all other lineages in early 2021. However, a series of variants (mostly containing the spike E484K mutation) defied these trends and persisted at moderately increasing proportions. Accounting for sustained introductions, however, indicates that their transmissibility is unlikely to exceed that of B.1.1.7. Finally, B.1.617.2 was repeatedly introduced to England and grew rapidly in April 2021, constituting approximately 40% of sampled COVID-19 genomes on May 15.

biorxiv; 2020.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2020.12.29.424619


The emergence of SARS-CoV-2 has resulted in a global pandemic. In addition to respiratory complications as a result of SARS-CoV-2 illness, accumulating evidence suggests that neurological and neuropsychiatric symptoms are associated with the disease caused by the virus. In this study, we investigated the effects of the SARS-CoV-2 spike glycoprotein S1 stimulation on neuroinflammation in BV-2 microglia. Analyses of culture supernatants revealed an increase in the production of TNF, IL-6, IL-1{beta} and iNOS/NO. SARS-CoV-2 spike glycoprotein S1 increased protein expressions of phospho-p65 and phospho-I{kappa}B, as well as enhancing DNA binding and transcriptional activity of NF-{kappa}B. Pro-inflammatory effects of the glycoprotein effects were reduced in the presence of BAY11-7082 (1 M). The presence of SARS-CoV-2 spike glycoprotein S1 in BV-2 microglia increased the protein expression of NLRP3, as well as caspase-1 activity. However, pre-treatment with CRID3 (1 M) or BAY11-7082 (1 M) resulted in the inhibition of NLRP3 inflammasome/caspase-1. It was also observed that CRID3 attenuated SARS-CoV-2 spike glycoprotein S1-induced increase in IL-1{beta} production. Increased protein expression of p38 MAPK was observed in BV-2 microglia stimulated with the spike glycoprotein S1, and was reduced in the presence of SKF 86002. These results have provided the first evidence demonstrating SARS-CoV-2 spike S1 glycoprotein-induced neuroinflammation in BV-2 microglia. We propose that promotion of neuroinflammation by this glycoprotein is mediated through activation of NF-{kappa}B, NLRP3 inflammasome and p38 MAPK. These results are significant because of their relevance to our understanding of neurological and neuropsychiatric symptoms observed in patients infected with SARS-CoV-2.

biorxiv; 2020.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2020.12.29.424712


ABSTRACT In 2020 we suffered from a major global pandemic caused by the SARS-CoV-2 coronavirus. Efforts to contain the virus include the development of rapid tests and vaccines, which require a ready supply of viral proteins. Here we report the production of two SARS-CoV-2 proteins by transient transformation of tobacco, leading to high expression within three days, and subsequent purification of the intact proteins. Such efforts may help to develop testing resources to alleviate the major impacts of this global pandemic.

medrxiv; 2020.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2020.08.26.20182279


Background COVID-19 poses a major challenge to infection control in care homes. SARS-CoV-2 is readily transmitted between people in close contact and causes disproportionately severe disease in older people. Methods Data and SARS-CoV-2 samples were collected from patients in the East of England (EoE) between 26th February and 10th May 2020. Care home residents were identified using address search terms and Care Quality Commission registration information. Samples were sequenced at the University of Cambridge or the Wellcome Sanger Institute and viral clusters defined based on genomic and time differences between cases. Findings 7,406 SARS-CoV-2 positive samples from 6,600 patients were identified, of which 1,167 (18.2%) were residents from 337 care homes. 30/71 (42.3%) care home residents tested at Cambridge University Hospitals NHS Foundation Trust (CUH) died. Genomes were available for 700/1,167 (60%) residents from 292 care homes, and 409 distinct viral clusters were defined. We identified several probable transmissions between care home residents and healthcare workers (HCW). Interpretation Care home residents had a significant burden of COVID-19 infections and high mortality. Larger viral clusters were consistent with within-care home transmission, while multiple clusters per care home suggested independent acquisitions.