SARS-CoV-2 Spike Protein Causes Heart Muscle Cell Injury

Researchers discovered that the spike protein from the SARS-CoV-2 virus can cause heart muscle injury during the inflammatory process. The preliminary findings of this study will be presented at the American Heart Association's Basic Cardiovascular Sciences Scientific Sessions 2022. The spike protein, which binds to angiotensin-converting enzyme 2 (ACE2) receptors on target cells, is identified on the surface of the virus that causes COVID-19.

Researchers Investigate SARS-CoV-2 Spike Protein

According to Nature, the SARS-CoV-2 spike protein interacts to the host cell receptor and causes viral-cell membrane fusion, which is essential for virus invasion and the initial stage of infection. In addition to attacking the lungs, the virus can travel to other organs, causing more damage, severe illness, and, in extreme cases, death.

Zhiqiang Lin, lead author of the study, said that it is already known from the clinical side that COVID-19 infection can cause heart injury. But they do not know the mechanism details of how it happens. He said that they suspect that the spike protein has unknown pathological roles. The findings indicate that the spike protein from SARS-CoV-2 causes cardiac muscle damage, which is why it's critical to get vaccinated and avoid this disease.

The researchers wanted to see if the SARS-CoV-2 spike protein triggered the body's normal immune response in cardiac muscle cells. HCoV-NL63 is a coronavirus that infects the respiratory system without causing cardiac damage, yet its spike protein similarly uses ACE2 to facilitate virus entrance. They investigated the ability of the SARS-CoV-2 spike protein and the NL63 spike protein to cause heart disease. Their findings demonstrated that the NL63 spike protein did not stimulate the body's innate immune response in cardiac muscle cells, whereas the SARS-CoV-2 spike protein did.

SARS-CoV-2 Spike Protein Research Findings

Researchers cloned the SARS-CoV-2 spike protein and the NL63 spike protein into the AAV9 viral vector to study the impact of the SARS-CoV-2 spike protein on the heart. To activate the spike protein in cardiac muscle cells, the AAV9 viral vector was administered into lab mice. They discovered that the SARS-CoV-2 spike protein, rather than the NL63 spike protein, was mediated by AAV9 and caused heart dysfunction, hypertrophic remodeling (enlargement), and cardiac inflammation.

In lab tests on heart cells cultivated in plates, researchers discovered that the SARS-CoV-2 spike protein caused heart muscle cells to grow significantly larger than those without either spike protein. Lin stated that they discovered direct proof that the SARS-CoV-2 spike protein is harmful to heart muscle cells.

During the investigation, researchers also looked at a heart biopsy from a deceased patient who had COVID-19 inflammation. They discovered the SARS-CoV-2 spike protein and the TLR4 protein in cardiac muscle cells as well as other cell types. In contrast, these two proteins were not found in a healthy human cardiac sample, which suggests that if the heart is infected with SARS-CoV-2, the TLR4 signaling will be activated. Aside from directly harming heart muscle cells, the spike protein itself is quite inflammatory and may create systemic inflammation, which may cause heart problems indirectly.

The researchers will now look into how SARS-CoV-2 spike proteins trigger cardiac inflammation.

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