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1.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-325235

ABSTRACT

Background: To compare the contingency modifications to the dental education between the University of Toronto Faculty of Dentistry and the Zhejiang University School of Stomatology during COVID-19 pandemic, and to share experiences in keeping the dental academic continuity, resuming practicing activities and preparing the faculty and students for a new normality. Three approaches were adopted to collect information and data: online interviews and email-contact with the instructors and the deans, a small-scale online survey of dental students, and official online announcements of various authorities. Results: : The two universities shared similarity in changing trends, while differed in details. The delivery of lectures, seminars and exams was transitioned from in-person mode to online mode and has proceeded effectively and efficiently. The pre-clinical lab training and clinical rotation were the most retarded parts and will not be resumed until the settle-down of the pandemic. Research activities have been kept on at the best possible level. Since the Zhejiang University reopened the campus in May 2020, clinical activities and research works were in recovery with a cautiously-planned and gradual phased approach. Conclusion: Both universities have been trying their best to meet the academic needs of students while protect their health, and to keep alert to the real time epidemic situation in preparation for resumption. Dental institutions could take the COVID-19 pandemic as an opportunity to armor dental students with infection control measures prior to their reengagement into clinical practice. There is a need of a new normality for global dental education that spans time and space.

2.
Social Behavior and Personality ; 49(11):1-12, 2021.
Article in English | ProQuest Central | ID: covidwho-1505081

ABSTRACT

Digital technologies significantly impact on manufacturing firms as they innovate their business processes in response to rapidly changing environments. Therefore, the proper use of digital technology to promote innovative behavior has become an important topic in research. However, few studies have examined how firm-level digital transformation affects individual-level innovative behavior. Drawing on the minority dissent perspective, we explored the mechanism by which digital transformation affects innovative behavior. Surveying 540 participants from Chinese manufacturing firms revealed that firm-level digital transformation was significantly correlated with both cross-functional minority dissent and individual-level innovative behavior. Moreover, minority dissent played a partial mediating role in the relationship between digital transformation and innovative behavior. This study sheds new light on how firm-level digital transformation can determine individual-level innovative behavior.

3.
J Virol ; 96(1): e0149221, 2022 01 12.
Article in English | MEDLINE | ID: covidwho-1476391

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an in silico investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both in vitro and in vivo. In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. IMPORTANCE There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity.


Subject(s)
Angiotensin-Converting Enzyme 2/genetics , COVID-19/genetics , Genetic Predisposition to Disease/genetics , Angiotensin-Converting Enzyme 2/metabolism , Genetic Variation , Humans , Polymorphism, Single Nucleotide , Protein Binding , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Spike Glycoprotein, Coronavirus/metabolism , Virus Internalization
4.
PLoS Pathog ; 17(3): e1009392, 2021 03.
Article in English | MEDLINE | ID: covidwho-1148252

ABSTRACT

Coronavirus interaction with its viral receptor is a primary genetic determinant of host range and tissue tropism. SARS-CoV-2 utilizes ACE2 as the receptor to enter host cell in a species-specific manner. We and others have previously shown that ACE2 orthologs from New World monkey, koala and mouse cannot interact with SARS-CoV-2 to mediate viral entry, and this defect can be restored by humanization of the restrictive residues in New World monkey ACE2. To better understand the genetic determinants behind the ability of ACE2 orthologs to support viral entry, we compared koala and mouse ACE2 sequences with that of human and identified the key residues in koala and mouse ACE2 that restrict viral receptor activity. Humanization of these critical residues rendered both koala and mouse ACE2 capable of binding the spike protein and facilitating viral entry. Our study shed more lights into the genetic determinants of ACE2 as the functional receptor of SARS-CoV-2, which facilitates our understanding of viral entry.


Subject(s)
COVID-19/enzymology , COVID-19/genetics , Peptidyl-Dipeptidase A/genetics , Receptors, Virus/genetics , SARS-CoV-2/physiology , Animals , Base Sequence , COVID-19/virology , Host Specificity , Humans , Mice/genetics , Mice/virology , Peptidyl-Dipeptidase A/chemistry , Peptidyl-Dipeptidase A/metabolism , Phascolarctidae/genetics , Phascolarctidae/virology , Receptors, Virus/metabolism , SARS-CoV-2/genetics , Sequence Alignment , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/metabolism , Virus Internalization
5.
Proc Natl Acad Sci U S A ; 118(12)2021 03 23.
Article in English | MEDLINE | ID: covidwho-1117490

ABSTRACT

The pandemic of COVID-19, caused by SARS-CoV-2, is a major global health threat. Epidemiological studies suggest that bats (Rhinolophus affinis) are the natural zoonotic reservoir for SARS-CoV-2. However, the host range of SARS-CoV-2 and intermediate hosts that facilitate its transmission to humans remain unknown. The interaction of coronavirus with its host receptor is a key genetic determinant of host range and cross-species transmission. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as the receptor to enter host cells in a species-dependent manner. In this study, we characterized the ability of ACE2 from diverse species to support viral entry. By analyzing the conservation of five residues in two virus-binding hotspots of ACE2 (hotspot 31Lys and hotspot 353Lys), we predicted 80 ACE2 proteins from mammals that could potentially mediate SARS-CoV-2 entry. We chose 48 ACE2 orthologs among them for functional analysis, and showed that 44 of these orthologs-including domestic animals, pets, livestock, and animals commonly found in zoos and aquaria-could bind the SARS-CoV-2 spike protein and support viral entry. In contrast, New World monkey ACE2 orthologs could not bind the SARS-CoV-2 spike protein and support viral entry. We further identified the genetic determinant of New World monkey ACE2 that restricts viral entry using genetic and functional analyses. These findings highlight a potentially broad host tropism of SARS-CoV-2 and suggest that SARS-CoV-2 might be distributed much more widely than previously recognized, underscoring the necessity to monitor susceptible hosts to prevent future outbreaks.


Subject(s)
Angiotensin-Converting Enzyme 2/genetics , COVID-19/veterinary , Receptors, Virus/genetics , SARS-CoV-2/genetics , Angiotensin-Converting Enzyme 2/metabolism , Animals , COVID-19/genetics , COVID-19/metabolism , COVID-19/virology , Host Specificity , Humans , Pandemics/prevention & control , Peptidyl-Dipeptidase A/genetics , Peptidyl-Dipeptidase A/metabolism , Phylogeny , Protein Binding , Receptors, Virus/metabolism , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/metabolism , Viral Tropism , Viral Zoonoses/genetics , Viral Zoonoses/prevention & control , Viral Zoonoses/virology , Virus Attachment , Virus Internalization
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