Researchers at a premier medical institution reported that after a coronavirus infection, the immune system can turn its attention to the body’s own tissues, sometimes harming healthy organs such as the heart. The findings, summarized in Circulation, reveal a chain of immune responses that can lead to inflammation and, in some cases, impaired heart function.
The investigators centered their work on cardiac macrophages, a type of immune cell that normally helps keep heart tissue strong and functioning smoothly. While these cells are essential guardians of heart health, they can also spark inflammation if they sense injury or if pre-existing heart conditions exist. In those moments, their activity may shift from protection to damage, contributing to adverse outcomes for heart tissue.
To explore what triggers this unwanted macrophage activity, researchers examined heart tissue from individuals who died with acute respiratory distress syndrome linked to SARS-CoV-2, alongside heart samples from individuals whose deaths were not related to COVID-19. The team also conducted experiments in mice, infecting them with SARS-CoV-2 to observe how macrophages respond over time after infection. These comparative studies helped distinguish virus-driven changes from other causes of heart disease.
The results showed an increase in the total number of cardiac macrophages in both human and mouse hearts following infection. Moreover, these cells exhibited abnormal behavior, producing inflammatory signals that contributed to inflammation within the heart. This cascade could damage cardiac tissue and impair its ability to pump effectively. The researchers noted that this inflammatory process in Covid-19 could also weaken other organs, underscoring the virus’s potential to affect multiple body systems.
Importantly, the team demonstrated that dampening the immune response in mice with a neutralizing antibody reduced the influx of inflammatory cardiac macrophages and helped preserve heart function. This finding suggests that targeted immune therapies might play a preventive role for patients with Covid-19 who have existing heart or metabolic conditions, possibly reducing the risk of complications. Such approaches could complement antiviral strategies and ongoing care to protect heart health during infection and recovery.
In a broader context, these observations contribute to a growing understanding of how viral infections can reprogram immune cells in the heart. They highlight the delicate balance between defending the body against pathogens and avoiding unintended damage to vital organs. Ongoing work aims to refine therapeutic options that can modulate immune responses without compromising the body’s ability to fight the virus, offering a potential path to safer outcomes for patients facing Covid-19 and related illnesses. (attribution: Circulation, as reported by Harvard Medical School researchers)
Earlier research has also identified genetic factors that influence heart function and disease risk. For instance, scientists have noted the existence of genes linked to heart failure, with ongoing studies exploring how these genetic components interact with immune pathways during infectious processes. This broader landscape helps explain why certain individuals may experience more pronounced cardiac effects when infected and points to future directions for precision medicine in cardiology. (attribution: peer-reviewed cardiac genetics literature)