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Captopril alleviates lung inflammation in SARS-CoV-2-infected hypertensive mice
Wen-Cong Gao1,2, Xin Ma1,2, Peng Wang1
1School of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan 650500, China.
Insights
Hypertension delayed SARS-CoV-2 replication in mice. Captopril treatment normalized replication but reduced lung inflammation, suggesting it may alleviate COVID-19 progression without impacting viral load.
Area of Science:
- Virology
- Cardiovascular Science
- Immunology
Background:
- The COVID-19 pandemic, caused by SARS-CoV-2, has been significantly influenced by cardiovascular comorbidities.
- Hypertension is a prevalent comorbidity that may impact COVID-19 outcomes.
Discussion:
- This study utilized a hypertensive mouse model to investigate the interplay between hypertension, SARS-CoV-2 infection, and antihypertensive treatment.
- SARS-CoV-2 replication was observed to be delayed in the lungs of hypertensive mice.
- Captopril treatment in hypertensive mice resulted in viral replication levels comparable to normotensive controls.
Key Insights:
- Antihypertensive therapy with captopril mitigated SARS-CoV-2-induced lung inflammation, including reduced interleukin-1β levels and immune cell infiltration.
- Hypertension itself did not exacerbate lung inflammation in SARS-CoV-2 infected mice compared to normotensive counterparts.
- Captopril treatment appears to alleviate COVID-19 progression markers without altering SARS-CoV-2 replication rates.
Outlook:
- Further research is warranted to explore the precise mechanisms by which captopril influences inflammation and disease progression in COVID-19.
- These findings may inform clinical strategies for managing hypertensive patients during the COVID-19 pandemic.
- Investigating other antihypertensive agents and their effects on SARS-CoV-2 infection is crucial.
Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent responsible for the global coronavirus disease 2019 (COVID-19) pandemic. Numerous studies have demonstrated that cardiovascular disease may affect COVID-19 progression. In the present study, we investigated the effect of hypertension on viral replication and COVID-19 progression using a hypertensive mouse model infected with SARS-CoV-2. Results revealed that SARS-CoV-2 replication was delayed in hypertensive mouse lungs. In contrast, SARS-CoV-2 replication in hypertensive mice treated with the antihypertensive drug captopril demonstrated similar virus replication as SARS-CoV-2-infected normotensive mice. Furthermore, antihypertensive treatment alleviated lung inflammation induced by SARS-CoV-2 replication (interleukin (IL)-1β up-regulation and increased immune cell infiltration). No differences in lung inflammation were observed between the SARS-CoV-2-infected normotensive mice and hypertensive mice. Our findings suggest that captopril treatment may alleviate COVID-19 progression but not affect viral replication.
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