New research demonstrates how influenza can directly damage the heart, leading to long-lasting cardiac dysfunction even after the lung infection clears. The study reveals that severe influenza A virus infection causes specialized immune cells to ferry the virus to heart muscle cells, unleashing harmful inflammatory signals.
Scientists identified a specific subset of immune cells, pro-dendritic cell 3 (pro-DC3), which become infected in the lungs. These virus-laden cells are then attracted to the heart. Once in the heart muscle, the virus escapes these immune cells and infects cardiomyocytes, heart muscle cells. This triggers the production of type-I interferon (IFN-I), a key antiviral molecule. However, excessive IFN-I signaling directly damages heart tissue and impairs pumping efficiency.
Crucially, this cardiac damage can be prevented without compromising the lungs' antiviral defenses. The study showed that targeted interventions blocking excessive interferon signaling specifically in heart tissue could protect against influenza-induced heart damage during severe infections. This opens possibilities for cardioprotective strategies to reduce long-term heart failure risk following severe respiratory infections.