tetano
Editor, Senior Moderator
Acta Cardiol Sin
. 2021 Nov;37(6):643-647.
doi: 10.6515/ACS.202111_37(6).20210726B.
The S Protein of SARS-CoV-2 Injures Cardiomyocytes Indirectly through the Release of Cytokines Instead of Direct Action
Wei-Ting Chang[SUP] 1 2 3 [/SUP], Yu-Wen Lin[SUP] 1 [/SUP], Zhih-Cherng Chen[SUP] 1 [/SUP], Ping-Yen Liu[SUP] 1 4 [/SUP]
Affiliations
Abstract
Background: Emerging evidence has shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with cardiac injury, but it remains unclear whether cardiac injury is mainly caused by direct viral infection or is secondary to SARS-CoV-2-induced cytokine storm.
Methods: Through directly treating cardiomyocytes with S protein, a crucial surface protein of SARS-CoV-2, and indirectly treating cardiomyocytes with S protein-derived human T lymphocyte conditioned medium, we compared the intensities of cardiomyocyte injuries caused by either S protein of the virus or S protein of virus-triggered cytokines.
Results: The directly treated cardiomyocytes did not show increasing cell apoptosis. In contrast, cardiomyocytes treated with the supernatant medium of S protein pre-conditioned peripheral blood mononuclear cells showed significantly suppressed viability. In addition, using a cardiovascular disease-specific PCR array, genes associated with hypertrophy, apoptosis, inflammation and angiogenesis were observed to be affected by cytokine stress.
Conclusions: Collectively, we found that SARS-CoV-2-induced heart injury may be mainly through the S protein of the virus enhancing host immune responses instead of the S protein of the virus per se. With regards to clinical application, the strategy for treating COVID-19 should not only focus on anti-viral therapy but also on suppressing over-activated immunity.
Keywords: Cardiac injury; Cytokine; S protein; SARS-CoV-2.
. 2021 Nov;37(6):643-647.
doi: 10.6515/ACS.202111_37(6).20210726B.
The S Protein of SARS-CoV-2 Injures Cardiomyocytes Indirectly through the Release of Cytokines Instead of Direct Action
Wei-Ting Chang[SUP] 1 2 3 [/SUP], Yu-Wen Lin[SUP] 1 [/SUP], Zhih-Cherng Chen[SUP] 1 [/SUP], Ping-Yen Liu[SUP] 1 4 [/SUP]
Affiliations
- PMID: 34812238
- PMCID: PMC8593489
- DOI: 10.6515/ACS.202111_37(6).20210726B
Abstract
Background: Emerging evidence has shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with cardiac injury, but it remains unclear whether cardiac injury is mainly caused by direct viral infection or is secondary to SARS-CoV-2-induced cytokine storm.
Methods: Through directly treating cardiomyocytes with S protein, a crucial surface protein of SARS-CoV-2, and indirectly treating cardiomyocytes with S protein-derived human T lymphocyte conditioned medium, we compared the intensities of cardiomyocyte injuries caused by either S protein of the virus or S protein of virus-triggered cytokines.
Results: The directly treated cardiomyocytes did not show increasing cell apoptosis. In contrast, cardiomyocytes treated with the supernatant medium of S protein pre-conditioned peripheral blood mononuclear cells showed significantly suppressed viability. In addition, using a cardiovascular disease-specific PCR array, genes associated with hypertrophy, apoptosis, inflammation and angiogenesis were observed to be affected by cytokine stress.
Conclusions: Collectively, we found that SARS-CoV-2-induced heart injury may be mainly through the S protein of the virus enhancing host immune responses instead of the S protein of the virus per se. With regards to clinical application, the strategy for treating COVID-19 should not only focus on anti-viral therapy but also on suppressing over-activated immunity.
Keywords: Cardiac injury; Cytokine; S protein; SARS-CoV-2.