Researchers hailing from the Centenary Institute and the University of Technology Sydney (UTS) have engineered a human heart cell model which reveals that the virus responsible for COVID-19 (SARS-CoV-2) possesses the ability to directly infect cardiac tissue. This discovery offers fresh insights into the reasons behind severe heart complications experienced by some individuals both during and following the infection.
These findings surface amidst the ongoing impact of COVID-19 on the health of Australians, with the country registering over 185,000 confirmed cases across the past year, according to data from the National Notifiable Diseases Surveillance System.
The study, featured in the journal Biofabrication, utilized minuscule, beating clusters of human heart cells, known as cardiac spheroids or “mini-hearts,” which mimic actual human heart tissue more closely than conventional laboratory cell models. Employing this 3D system, the research team demonstrated that the SARS-CoV-2 virus can directly infiltrate heart tissue, subsequently triggering damaging inflammation and alterations associated with impaired heart function.
“When we commenced this research at the pandemic’s onset, it was uncertain whether COVID-19 exerted harm on the heart indirectly via inflammation and the immune system, or directly by infecting the heart cells themselves,” commented study co-author Matt Johansen, affiliated with both the Centenary Institute and the University of Technology Sydney. “Our results confirm that the virus can, under specific circumstances, directly invade human heart tissue and initiate detrimental processes. This may account for the significant concern surrounding cardiac complications in COVID-19 cases, even among individuals with no prior history of heart disease.”
Co-author Clara Liu Chung Ming noted that the team determined SARS-CoV-2 could successfully infect and replicate within the three-dimensional heart tissue model, yet this capability was absent when tested against individual heart cell types cultured in isolation.
“This underscores the crucial nature of examining heart cells within a model that accurately reflects their spatial arrangement in the human heart,” stated Liu Chung Ming. “Furthermore, it indicates that the manner in which diverse heart cells interact and communicate plays a vital role in how COVID-19 infection might cause cardiac damage. This physiologically relevant model provides us with a novel avenue to comprehend what could be occurring in patients, including those suffering from lingering heart symptoms post-COVID-19.”
Study co-author Carmine Gentile from the University of Technology Sydney stated that this model is instrumental in establishing a foundation for devising new protective strategies for the heart against COVID-19, as well as against other viral threats.
“This could prove to be an invaluable asset for screening forthcoming treatments and for preventing or mitigating heart damage caused by viral infections,” Gentile said. “By grasping precisely how viruses can compromise the heart, we will be in a better position to enhance the care provided to those affected by COVID-19 and to prepare more effectively for future pandemics.”
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