Inhibition of the Cellular Deubiquitinase UCHL1 Suppresses SARS-CoV-2 Replication

Larabee et al aimed to investigate the role of UCHL1 in regulating the infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19. They used an in vitro model of the human airway epithelium to study the effects of ubiquitin C-terminal hydrolase 1 (U...

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Published inAmerican journal of respiratory cell and molecular biology Vol. 69; no. 3; pp. 367 - 370
Main Authors Subramaniyan, Bharathiraja, Larabee, Jason L., Bodas, Manish, Moore, Andrew R., Burgett, Anthony W. G., Papin, James F., Walters, Matthew S.
Format Journal Article
LanguageEnglish
Published New York American Thoracic Society 01.09.2023
Subjects
ACE2
Angiotensin-converting enzyme 2
Cell differentiation
Cells
Coronaviruses
Correspondence
COVID-19
Epithelial cells
Epithelium
Human papillomavirus
Immune response
Innate immunity
Keratinocytes
Medical treatment
Protein gene product 9.5
Replication
Respiratory tract
Severe acute respiratory syndrome coronavirus 2
Therapeutic applications
Ubiquitin
Ubiquitin carboxy-terminal hydrolase
Viral infections
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Summary:Larabee et al aimed to investigate the role of UCHL1 in regulating the infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19. They used an in vitro model of the human airway epithelium to study the effects of ubiquitin C-terminal hydrolase 1 (UCHL1) overexpression on SARS-CoV-2 replication. They generated a stable cell line that overexpresses UCHL1 and found that this overexpression did not have any negative effects on the differentiation of airway epithelial cells. Additionally, they observed that UCHL1 overexpression did not lead to increased levels of ACE2, the receptor through which SARS-CoV-2 enters cells. These findings suggest that UCHL1 may not play a significant role in promoting SARS-CoV-2 infection. Furthermore, they found that UCHL1 upregulation during human papillomavirus infection of keratinocytes suppresses the innate immune response, potentially promoting virus replication. Overall, the study provides insights into the role of UCHL1 in viral infections and highlights its potential as a target for therapeutic interventions.
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These authors contributed equally to this work.
ISSN:1044-1549
1535-4989
DOI:10.1165/rcmb.2023-0076LE