Researchers, including those of Indian-origin, have shown that the novel coronavirus can infect lab-grown cardiac muscle cells, indicating it may be possible for the virus to directly cause heart infection in COVID-19 patients.
The study, published in the journal Cell Reports Medicine, was based on experiments conducted in lab-grown heart muscle cells which were produced from unspecialised human stem cells.
"We not only uncovered that these stem cell-derived heart cells are susceptible to infection by novel coronavirus, but that the virus can also quickly divide within the heart muscle cells," said study co-author Arun Sharma from the Cedars-Sinai Board of Governors Regenerative Medicine Institute in the United States.
"Even more significant, the infected heart cells showed changes in their ability to beat after 72 hours of infection," Sharma said.
Although many COVID-19 patients experience heart problems, the scientists said the reasons for these symptoms are not entirely clear.
They said pre-existing cardiac conditions, or inflammation and oxygen deprivation that result from the infection have all been implicated.
According to the scientists, there is only limited evidence available that the novel coronavirus, SARS-CoV-2, directly infects individual muscle cells of the heart.
The current study showed that SARS-CoV-2 can infect heart cells derived from human stem-cells and change how the genes in these cells helped make proteins.
Based on this observation, the scientists confirmed that human heart cells can be actively infected by the virus, activating innate cellular 'defense mechanisms' in an effort to help clear out the virus.
Citing the limitations of the study, they said these findings are not a perfect replicate of what is happening in the human body since the research was carried out in lab-grown heart cells.
However, this knowledge may help investigators use stem cell-derived heart cells as a screening platform to identify new antiviral compounds that could alleviate viral infection of the heart, believes study co-author Clive Svendsen.
"This viral pandemic is predominately defined by respiratory symptoms, but there are also cardiac complications, including arrhythmias, heart failure and viral myocarditis," said Svendsen, director of the Regenerative Medicine Institute.
"While this could be the result of massive inflammation in response to the virus, our data suggest that the heart could also be directly affected by the virus in COVID-19," Svendsen said.
The scientists also found that treatment with an antibody protein could lock onto the human cell surface receptor ACE2 -- a known SARS-CoV-2 'gateway' into cells.
According to the researchers, the antibody treatment was able to blunt viral replication on the lab-grown heart cells, suggesting that the ACE2 receptor could be used by the virus to enter human heart muscle cells.
"By blocking the ACE2 protein with an antibody, the virus is not as easily able to bind to the ACE2 protein, and thus cannot easily enter the cell," Sharma said.
"This not only helps us understand the mechanisms of how this virus functions, but also suggests therapeutic approaches that could be used as a potential treatment for SARS-CoV-2 infection," he added.
In the study, the researchers also used human induced pluripotent stem cells, or iPSCs, which are a type of undifferentiated cells grown in the lab from a person's blood or skin cells.
They said iPSCs can make any cell type found in the body, each one carrying the genetic material of the individual.
According to the scientists, tissue-specific cells created in this way are used for research, and for creating and testing potential disease treatments.
"It is plausible that direct infection of cardiac muscle cells may contribute to COVID-related heart disease," said Eduardo Marban, executive director of the Smidt Heart Institute in the US, and study co-author.
"This key experimental system could be useful to understand the differences in disease processes of related coronaviral pathogens, SARS and MERS," said Vaithilingaraja Arumugaswami, another co-author of the study from the University of California Los Angeles in the US.
