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Published on: December 23, 2020
Renin-angiotensin system in human coronavirus pathogenesis
Brigitte A Wevers1, Lia van der Hoek2
1Center for Experimental & Molecular Medicine, Center for Infection & Immunity Amsterdam, Academic Medical Center, University of Amsterdam, PO Box 226600, 1100 DD Amsterdam, The Netherlands. b.a.wevers@amc.uva.nl.
Human coronaviruses (HCoVs), including NL63 and HKU1, can cause severe illness. This review explores how the renin-angiotensin system aids HCoV entry and pathogenesis.
Area of Science:
- Virology
- Pathogenesis
- Molecular Biology
Background:
- Human coronaviruses (HCoVs) were once underestimated but are now recognized for causing severe clinical issues.
- The pathogenic potential of HCoVs, especially newer strains like HCoV-NL63 and HCoV-HKU1, remains incompletely understood.
- HCoV infection relies on host cell proteins for successful replication.
Purpose of the Study:
- To review current knowledge on the role of the renin-angiotensin system in HCoV pathogenesis.
- To elucidate the function of renin-angiotensin system proteases as cellular receptors for HCoV entry.
Main Methods:
- Literature review of existing research on HCoV pathogenesis and the renin-angiotensin system.
- Analysis of studies investigating host-pathogen interactions involving HCoVs and cellular proteases.
Main Results:
- Renin-angiotensin system proteases are identified as crucial receptors for HCoV entry into target cells.
- The renin-angiotensin system plays a significant role in the pathogenesis of HCoV infections.
- Specific HCoVs, including HCoV-NL63 and HCoV-HKU1, utilize these pathways for cellular invasion.
Conclusions:
- The renin-angiotensin system is a key factor in HCoV pathogenesis, acting as an entry point for the virus.
- Understanding this interaction is vital for developing strategies against severe HCoV infections.
- Further research is needed to fully characterize the pathogenic mechanisms of emerging HCoVs.
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