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SARS-CoV-2 has continued spreading around the world in recent years since the initial outbreak in 2019, frequently developing into new variants with greater human infectious capacity. SARS-CoV-2 and its mutants use the angiotensin-converting enzyme 2 (ACE2) as a cellular entry receptor, which has triggered several therapeutic strategies against COVID-19 relying on the use of ACE2 recombinant proteins as decoy receptors. In this work, we propose an ACE2 silent Fc fusion protein (ACE2-hFcLALA) as a candidate therapy against COVID-19.

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In one of the earliest reports from China during COVID-19, it was noted that over 20% of patients hospitalized with the disease had significant elevations of troponin, a marker of myocardial tissue damage, that put them at a higher risk. In a hypothesis-independent whole exome sequencing (WES) study in hospitalized COVID-19 patients of diverse ancestry, we observed putative enrichment in pathogenic variants in genes known to be involved in the pathogenesis of cardiomyopathy. This observation led us to hypothesize that the observed high morbidity and mortality in these patients might be due to the presence of rare genetic factors that had previously been silent but became relevant as a consequence of the severe stress inflicted by an infection with SARS-CoV-2.

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Background: Pulmonary fibrosis (PF) is a frequently reported COVID-19 sequela. It is a progressive disorder characterized by respiratory failure and death. The properties of Alpinia officinarum Rhizomes (AO) make it a highly potent antioxidant, anti-inflammatory, and antifibrotic agent.

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To test or not to test? A new behavioral epidemiology framework for COVID-19.

PLoS One

December 2024

School of Economics and Finance, Queensland University of Technology, Brisbane, QLD, Australia.

Evidence from clinical research suggests that in the first two waves of COVID-19, the virus spread rapidly through a large number of undocumented asymptomatic infections. These 'silent' infections camouflaged the actual incidence of the disease, leading to downward biases in the rates of transmission, disease prevalence, and fatality. These, in turn, had implications for how people and policymakers responded to changing infection prevalence.

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