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Cathepsins and SARS-CoV-2 infection: From pathogenic factors to potential therapeutic targets
Shuxuan Zhao1, Muzhou Jiang2, Hong Qing1
1Key Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, China.
Insights
Lysosomal cathepsins play a role in COVID-19 pathogenesis and immune responses. Targeting these enzymes offers a potential therapeutic strategy for severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection.
Area of Science:
- Biochemistry
- Immunology
- Virology
Background:
- Coronavirus disease-19 (COVID-19), caused by SARS-CoV-2, lacks specific treatments.
- Lysosomal cathepsins are implicated in COVID-19 pathogenesis and disease severity.
Purpose of the Study:
- To review current evidence on cathepsins' pathological roles in SARS-CoV-2 infection.
- To explore underlying mechanisms of cathepsin involvement in host immune dysregulation.
- To discuss cathepsin-based therapeutic strategies for COVID-19.
Main Methods:
- Literature review of preclinical and clinical studies.
- Analysis of the role of cathepsins in viral pathogenesis.
- Discussion of enzyme inhibitor strategies.
Main Results:
- Cathepsins contribute to SARS-CoV-2 infection progression.
- These enzymes are involved in host immune system dysregulation during infection.
- Cathepsins' substrate-binding pockets are suitable for inhibitor development.
Conclusions:
- Cathepsin activity modulation is a promising therapeutic avenue for COVID-19.
- Targeting cathepsins could lead to novel interventions against SARS-CoV-2.
- Further research into cathepsin-based therapies is warranted.
Abstract:
Coronavirus disease-19 (COVID-19) is caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. The COVID-19 pandemic began in March 2020 and has wrought havoc on health and economic systems worldwide. Efficacious treatment for COVID-19 is lacking: Only preventive measures as well as symptomatic and supportive care are available. Preclinical and clinical studies have indicated that lysosomal cathepsins might contribute to the pathogenesis and disease outcome of COVID-19. Here, we discuss cutting-edge evidence on the pathological roles of cathepsins in SARS-CoV-2 infection, host immune dysregulations, and the possible underlying mechanisms. Cathepsins are attractive drug targets because of their defined substrate-binding pockets, which can be exploited as binding sites for pharmaceutical enzyme inhibitors. Accordingly, the potential modulatory strategies of cathepsin activity are discussed. These insights could shed light on the development of cathepsin-based interventions for COVID-19.
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