Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
SARS-CoV-2 virus causes upper and lower respiratory diseases including pneumonia, and in some cases, leads to lethal pulmonary failure. Angiotensin converting enzyme-2 (ACE2), the receptor for cellular entry of SARS-CoV-2 virus, has been shown to protect against severe acute lung failure. Here, we provide evidence that SARS-CoV-2 spike protein S1 reduced the mRNA expression of ACE2 and type I interferons in primary cells of lung bronchoalveolar lavage (BAL) from naïve rhesus macaques. The expression levels of ACE2 and type I interferons were also found to be correlated with each other, consistent with the recent finding that ACE2 is an interferon-inducible gene. Furthermore, induction of ACE2 and type I interferons by poly I:C, an interferon inducer, was suppressed by S1 protein in primary cells of BAL. These observations suggest that the downregulation of ACE2 and type I interferons induced by S1 protein may directly contribute to SARS-CoV-2-associated lung diseases.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8213020 | PMC |
| http://dx.doi.org/10.3389/fimmu.2021.658428 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
COVID-19-Induced Flare of Hereditary Angioedema in a Twelve-Year-Old Female Patient.
Cureus
August 2025
Allergy and Immunology, Case Western Reserve University/University Hospitals Cleveland Medical Center Program, Cleveland, USA.
Hereditary angioedema (HAE) is a rare disorder characterized by recurrent episodes of angioedema, most often due to a deficiency or dysfunction of C1 esterase inhibitor. This deficiency leads to an accumulation of bradykinin, a pro-inflammatory peptide that increases vascular permeability and causes localized swelling. Although some HAE flares occur spontaneously, known triggers include trauma, stress, and infection.
View Article and Find Full Text PDFThe Tetraspanin CD9 Facilitates SARS-CoV-2 Infection and Brings Together Different Host Proteins Involved in SARS-CoV-2 Attachment and Entry into Host Cells.
Viruses
August 2025
Department of Molecular and Cell Biology, Centro Nacional de Biotecnología-Consejo Superior de Investigaciones Científicas (CNB-CSIC), 28049 Madrid, Spain.
CD9 protein belongs to a family of proteins called tetraspanins, so named for their four-transmembrane-spanning architectures. These proteins are located in domains in the plasmatic membrane, called tetraspanin-enriched microdomains (TEMs). Several proteases and cellular receptors for virus entry cluster into TEMs, suggesting that TEMs are preferred virus entry portals.
View Article and Find Full Text PDFAngiotensin-(1-7) Mitigates Progression from Acute Kidney Injury to Chronic Kidney Disease Via Renin-Angiotensin System Modulation in a Murine Model.
Inflammation
August 2025
Department of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China.
Acute kidney injury (AKI) often progresses to chronic kidney disease (CKD), presenting a significant clinical challenge. The renin-angiotensin system (RAS), particularly the protective arm involving Angiotensin-(1-7) (Ang-(1-7)), offers a potential therapeutic target to mitigate this progression. This study explores the effects of Ang-(1-7) in a murine model of ischemia-reperfusion (I/R) injury-induced AKI.
View Article and Find Full Text PDFSMAD5 phosphorylation by ALK1 is modulated by the interaction of the spike protein of SARS-CoV-2 and angiotensin-converting enzyme 2.
Antiviral Res
October 2025
Department of Intractable Diseases, National Institute of Global Health and Medicine, Japan Institute for Health Security, 1-21-1 Toyama, Shinjuku-ku, Tokyo, 162-8655, Japan. Electronic address:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused more than 7 million worldwide deaths, but the mechanisms underlying its severe clinical outcomes remain elusive. Although attachment of the spike (S) protein of SARS-CoV-2 to angiotensin-converting enzyme 2 (ACE2), a pivotal step for infection, induces inflammation, the intracellular signals triggered by this interaction are unclear. Here, we found that S protein induced phosphorylation of SMAD family member 5 which was mediated by the bone morphologenetic protein (BMP) receptor activin receptor-like kinase 1 (ALK1) and BMP receptor type II.
View Article and Find Full Text PDFSARS-CoV-2 XBB.1.5 infects wild-type C57BL/6 mice and induces a protective CD4 T cell response required for viral clearance.
Front Cell Infect Microbiol
August 2025
Department of Biology, College of Arts and Sciences, Georgia State University, Atlanta, GA, United States.
Mouse models are critical for studying SARS-CoV-2 pathogenesis and evaluating therapeutic and preventive strategies. Standard C57BL/6 mice are generally resistant to infection with the ancestral SARS-CoV-2 strain due to inefficient binding of the viral spike protein to the murine angiotensin-converting enzyme 2 (ACE2) receptor. Although human ACE2 transgenic mice can support robust pulmonary infection, these models often develop fatal encephalitis, a pathology not commonly observed in humans.
View Article and Find Full Text PDF