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Basic Characteristics of Mutations
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Mutation Site
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D614G |
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Mutation Site Sentence
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Notably, in regions of the epithelium showing clear signs of infection with the D614G variant at an MOI of 1, as indicated by the dsRNA signal, the pattern of ZO1 expression remained unchanged. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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Standardized Encoding Gene
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Genotype/Subtype
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- |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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COVID-19
Cystic Fibrosis
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Immune
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- |
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
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- |
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Location
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- |
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Literature Information
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PMID
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39311876
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Title
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Distinct Responses of Cystic Fibrosis Epithelial Cells to SARS-CoV-2 and Influenza A Virus
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Author
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Pagani I,Venturini A,Capurro V,Nonis A,Ghezzi S,Lena M,Alcala-Franco B,Gianferro F,Guidone D,Colombo C,Pedemonte N,Bragonzi A,Cigana C,Galietta LJV,Vicenzi E
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Journal
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American journal of respiratory cell and molecular biology
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Journal Info
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2025 Mar;72(3):308-319
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Abstract
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The coronavirus disease (COVID-19) pandemic has underscored the impact of viral infections on individuals with cystic fibrosis (CF). Initial observations suggested lower COVID-19 rates among CF populations; however, subsequent clinical data have presented a more complex scenario. This study aimed to investigate how bronchial epithelial cells from individuals with and without CF, including various CFTR (CF transmembrane conductance regulator) mutations, respond to in vitro infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants and SARS-CoV. Comparisons with the influenza A virus (IAV) were included based on evidence that patients with CF experience heightened morbidity from IAV infection. Our findings showed that CF epithelial cells exhibited reduced replication of SARS-CoV-2, regardless of the type of CFTR mutation or SARS-CoV-2 variant, as well as the original 2003 SARS-CoV. In contrast, these cells displayed more efficient IAV replication than non-CF cells. Interestingly, the reduced susceptibility to SARS-CoV-2 in CF was not linked to the expression of ACE2 (angiotensin-converting enzyme 2) receptor or to CFTR dysfunction, as pharmacological treatments to restore CFTR function did not normalize the viral response. Both SARS-CoV-2 infection and CFTR function influenced the concentrations of certain cytokines and chemokines, although these effects were not correlated. Overall, this study reveals a unique viral response in CF epithelial cells, characterized by reduced replication for some viruses like SARS-CoV-2, while showing increased susceptibility to others, such as IAV. This research offers a new perspective on CF and viral interactions, emphasizing the need for further investigation into the mechanisms underlying these differences.
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Sequence Data
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-
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