Do not take it lightly!"Science" sub -magazine found that influenza virus may directly cause heart damage

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Do not take it lightly!"Science" sub -magazine found that influenza virus may directly cause heart damage

2022-05-16 12:14:52 24 ℃

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After a cold, do many people basically don't take it seriously, a little nose, and the cough stands up? Really fever or more serious only to go to the hospital for medicine and injections. However, a latest study of "Science-Progress" reminds that if it is not a normal cold, but the cold symptoms caused by the influenza virus, the consequences are likely to be serious, and even direct damage to the heart.

Some of the past studies have speculated that the heart problems related to influenza may be caused by lung inflammation, but the research team of Ohio State University has confirmed through mice that the cardiac telecommunications signal disorders and myocardial damage to the influenza patients are confirmed. It is caused by infected heart cells.

In fact, the probability of heart problems with influenza patients is not low. According to a report released by the US CDC last year, one of each 8 patients in the hospital may have heart problems.

Some of the past studies by Professor Jacob Yount University of Ohio State also reminded this possibility. He and his colleagues have found influenza virus particles in the mouse heart cells infected with influenza.

Picture source: 123RF

In new research, they further promoted the progress of related research. Based on past genetic analysis experience, they have built a group of mice that lack key immune gene ifitm3. IFITM3 can encode a protein in a congenital immune system and can effectively fight virus infection.

Mouses that lack iFitm3 expressions will be more prone to heart problems after infection. Not only are they highly susceptible to influenza virus, but they also lack some antiviral infection proteins. The proportion of IFITM3 expression in different people is about 4%-20%, which means that many people themselves will be more likely to be infected by viruses.

Subsequently, the research transformed the H1N1 influenza virus, and these mutant influenza viruses could not be copied in the heart cells. They injected the control viruses and transform viruses into ordinary mice and IFITM3 defective mice.

After a period of time, both viruses will cause severe lung and systemic inflammation of mice, and they can also detect a large number of viruses in their bodies. However, ordinary mice with defective influenza viruses have no virus particles in their heart cells, and IFITM3 defective mice with weak resistance ability, their hearts only have very low concentration of defect virus particles.

▲ The mice that injected the defect virus, and they include multiple indicators, including the cardiac telecommunications signal, will not appear abnormal (picture source: reference materials [2])

These infected virus mice have less myocardial damage, and the degree of fibrosis and scar in the cardiac tissue is also very low, and there is no abnormal electrical signal problem. Professor Yount explained: "We use these defective viruses and mice to distinguish the pneumonia caused by influenza and heart problems. The heart without active replication of the heart will not cause heart damage."

Studies have pointed out that influenza viruses tend to concentrate in the lungs instead of existing in blood or other organs, but it can accidentally attack the heart. This shows that it is necessary to reduce the number of viruses in a timely manner after a cold and prevent heart problems.

Of course, there are some problems in the research team to solve in the future. Will these influenza viruses enter the heart kill cells? Will it have a long -term impact on cardiac function? If so, the impact of a cold may really be more serious than expected, and it is worthy of our vigilance!

Reference materials:

[1] Flu Causes Cautiac Complications by Directly Infecting the Heart. RERIEVED May 12th, 2022 from

[2] Adam D. Kenney et al, Influenza Virus Replication in Cardiomyocytes Drives Heart Dysfunction and Fibrosis, Science Advances (2022). Doi: 10.1126/Sciadv.abm5371.