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Characterization of SARS-CoV-2 Entry Genes in Skeletal Muscle and Impacts of In Vitro Versus In Vivo Infection.
J Cachexia Sarcopenia Muscle
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Meakins-Christie Laboratories and Translational Research in Respiratory Diseases Program, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
Background: COVID-19 has been associated with both respiratory (diaphragm) and non-respiratory (limb) muscle atrophy. It is unclear if SARS-CoV-2 infection of skeletal muscle plays a role in these changes. This study sought to: 1) determine if cells comprising skeletal muscle tissue, particularly myofibres, express the molecular components required for SARS-CoV-2 infection; 2) assess the capacity for direct SARS-CoV-2 infection and its impact on atrophy pathway genes in myogenic cells; and 3) in an animal model of COVID-19, examine the relationship between viral infection of skeletal muscle and myofibre atrophy within the diaphragm and limb muscles.
View Article and Find Full Text PDFDiverse strategies utilized by coronaviruses to evade antiviral responses and suppress pyroptosis.
Int J Biol Macromol
January 2025
Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou, China; Institute of Preventive Veterinary Medicine, Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, Zhejiang University, Hangzhou, China; Key Laboratory of Animal Virology of Ministry of Agriculture, Center for Veterinary Sciences, Zhejiang University, Hangzhou, China; Hainan Institute of Zhejiang University, Sanya, China; Zhejiang University-Xinchang Joint Innovation Centre (TianMu Laboratory), Gaochuang Hi-Tech Park, Xinchang, China. Electronic address:
Viral infections trigger inflammasome-mediated caspase-1 activation. Nevertheless, limited understanding exists regarding how viruses use the active caspase-1 to evade host immune response. Here, we use porcine epidemic diarrhea virus (PEDV) as a model of coronaviruses (CoVs) to illustrate the intricate regulation of CoVs to combat IFN-I signaling and pyroptosis.
View Article and Find Full Text PDFInteractomic Analyses and a Reverse Engineering Study Identify Specific Functional Activities of One-to-One Interactions of the S1 Subunit of the SARS-CoV-2 Spike Protein with the Human Proteome.
Biomolecules
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Unit of Medical Informatics-AOU Luigi Vanvitelli, University of Campania, 80138 Naples, Italy.
The S1 subunit of SARS-CoV-2 Spike is crucial for ACE2 recognition and viral entry into human cells. It has been found in the blood of COVID-19 patients and vaccinated individuals. Using BioGRID, I identified 146 significant human proteins that interact with S1.
View Article and Find Full Text PDFRegulation of N-degron recognin-mediated autophagy by the SARS-CoV-2 PLpro ubiquitin deconjugase.
Autophagy
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Department of Cell and Molecular Biology, Karolinska Institutet, Solna, Sweden.
Viral proteases play critical roles in the host cell and immune remodeling that allows virus production. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) papain-like protease (PLpro) encoded in the large nonstructural protein 3 (Nsp3) also possesses isopeptidase activity with specificity for ubiquitin and ISG15 conjugates. Here, we interrogated the cellular interactome of the SARS-CoV-2 PLpro catalytic domain to gain insight into the putative substrates and cellular functions affected by the viral deubiquitinase.
View Article and Find Full Text PDFPellino-1, a therapeutic target for control of SARS-CoV-2 infection and disease severity.
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Department of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA; Department of Pathology, University of Texas Medical Branch, Galveston, TX, USA. Electronic address:
Enhanced expression of Pellino-1 (Peli1), a ubiquitin ligase is known to be associated with COVID-19 susceptibility. The underlying mechanisms are not known. Here, we report that mice deficient in Peli1 (Peli1) had reduced viral load and attenuated inflammatory immune responses and tissue damage in the lung following SARS-CoV-2 infection.
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