New study suggests severe flu can damage the heart
A new study shows how the body’s response to severe influenza can kill heart muscle cells, a discovery that could pave the way for drugs to prevent heart damage.
- 16 February 2026
- 5 min read
- by Linda Geddes
At a glance
- Flu season has long been associated with an increase in deaths linked to heart disease, but the underlying mechanism has been unclear.
- A new study published in Immunity suggests that a poorly understood type of immune cell, known as pro-dendritic cell 3, acts as a kind of Trojan horse during severe influenza infection, carrying the virus to the heart.
- Influenza vaccination reduced heart damage in animal models, suggesting flu vaccines may help to protect not only the lungs but the heart as well.
Severe flu infections don’t just leave people coughing and feverish – they may also quietly damage the heart.
New research has shed light on how the body’s immune response to influenza inflicts this harm, raising hopes of new therapies to protect people with severe infections from heart attacks and other cardiovascular complications.
What’s the link between flu and heart disease?
Seasonal influenza infects around one billion people worldwide each year, with influenza A viruses responsible for a large share of those cases.
For most people, the infection is unpleasant but short-lived. But each winter, as flu begins to circulate, doctors see a familiar and troubling pattern: a rise in deaths linked to heart disease.
“We have known for years that the frequency of heart attacks increases during flu season, yet outside of clinical intuition, scant evidence exists of the underlying mechanisms of that phenomenon,” said Prof Filip Swirski, Director of the Cardiovascular Research Institute at the Icahn School of Medicine at Mount Sinai in New York, the study’s senior author.
Some researchers think the harm stems from widespread inflammation that causes collateral damage to the cardiovascular system. Others have proposed that the virus directly infects heart tissue and replicates there, triggering local injury.
To investigate, Swirski and colleagues analysed autopsy records from 35 patients who died of influenza, along with blood samples from hospitalised patients, looking for evidence of heart damage.
They then used mouse models of severe influenza A infection to trace the process step by step – tracking immune cells, measuring heart function and mapping how the virus moves through the body – to better understand how influenza can shift from a predominantly respiratory infection into one that harms the heart.
How does influenza trigger heart damage?
The research, published in Immunity, found that more than 85% of hospitalised patients who died of influenza had at least one significant cardiovascular condition, such as high blood pressure or atherosclerosis, and most had several.
While severe influenza often affects older people who may already have heart disease, further experiments suggest the relationship is not simply a coincidence: flu and cardiovascular disease appear to interact, each making the other more dangerous.
Blood tests from other hospitalised flu patients showed that more than 60% had biochemical signs of heart injury or strain.
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By contrast, fewer than 10% of patients hospitalised with severe ulcerative colitis – another serious inflammatory condition – showed similar abnormalities, supporting the idea that flu-related heart injury is not simply a consequence of serious illness or general inflammation.
Meanwhile, the mouse experiments showed that infected immune cells carry the virus from the lungs to the heart, where it briefly infects heart muscle.
But the virus itself does not appear to be the main driver of damage. Instead, infection triggers a powerful antiviral response involving a molecule called type I interferon – and it is this immune reaction that ultimately harms the organ.
At the centre of the process is a poorly understood type of immune cell, known as pro-dendritic cell 3. “We found that the pro-dendritic cell 3 acts as the ‘Trojan horse’ of the immune system during influenza infection, becoming infected in the lung, trafficking the virus to the hear, and disseminating it to cardiomyocytes,” said Dr Jeffrey Downey, who led the study.
Vaccinated mice experienced less cardiac damage and maintained better heart function after infection, even when the vaccine did not fully prevent illness.
“This process causes production of the damaging type 1 interferon that comes with considerable collateral damage to the heart.”
The team also discovered that pre-existing cardiovascular disease in the mice made influenza-related heart damage significantly worse, suggesting the two conditions amplify each other.
Could influenza-related heart damage be prevented?
The researchers tested whether influenza vaccination could protect the heart in their animal models and found that it did: vaccinated mice experienced less cardiac damage and maintained better heart function after infection, even when the vaccine did not fully prevent illness.
They also explored whether blocking the harmful immune response in the heart could prevent injury without weakening the body’s ability to fight the virus.
One approach switched off the receptor that allows heart cells to respond to interferon. Another used an experimental mRNA therapy that instructs heart cells to make a dummy version of that receptor, which blocks the signal.
When tested in mice, both strategies protected heart function while leaving the rest of the immune response largely intact.
“These findings offer great promise for the development of new therapies, which are desperately needed since there are currently no viable clinical options to prevent cardiac damage,” Swirski said.
The study also suggests that timing may be critical. Because the virus appears to be cleared from the heart early – often before symptoms develop – treatments that target the virus itself may arrive too late.
Instead, therapies that dampen the damaging immune response in the heart may need to be given early in severe infection, before inflammation takes hold.
They also highlight another benefit of vaccination: by reducing the severity of infection – even when it does not completely prevent illness – flu vaccines may interrupt the chain of events that leads to heart damage, helping protect not only the lungs but also the cardiovascular system.
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