Mechanisms of Influenza Driven Cardiac Dysfunction


Throughout recorded history, influenza virus has been an ever-present concern of mankind. Since the late 19th century, we’ve experienced 6 pandemics, the worst being in 1918.

Nearly 500 million people were infected, a third of world’s population at the time, and the virus claimed an estimated 50 million lives. Although the influenza virus mainly attacks the infected through the respiratory system, it can also bring about adverse cardiac complications.

During the 1918 influenza pandemic, 90% of those who succumbed to the virus also had varying degrees of myocardial damage. During other epidemics, less virulent strains of the virus have had a rate of 40–50%. It is hypothesized that more virulent influenza strains lead to more severe infections, which bring about higher incidences of cardiac damage and complications.

Scientists believe the influenza virus’ main pathway to the heart is through circulation, since severely infected individuals have a higher prevalence of the virus in their bloodstreams. While mounting clinical data affirms these hypotheses, much is still unknown about the mechanisms that allow influenza to cause damage to the heart.

In early 2021, JCVI’s Norberto Gonzalez-Juarbe, PhD and his team published a major manuscript in the journal Circulation Research, showing that the influenza virus is not only able to reach the heart, but still persists long after the infection has left the lungs. It’s the first evidence that suggests the cardiac proteome, or set of proteins in the heart, can be significantly altered during and after infection.

Building on these findings, Dr. Gonzalez-Juarbe is proposing a new project to further investigate how the influenza virus is able to cause inflammatory responses, mitochondrial damage, oxidative stress and necrotic cell death leading to cardiac injury and potential heart failure.

It is estimated that seasonal flu epidemics infect between 3-5 million people a year, with approximately 250,000-500,000 deaths. As we were reminded over the course of the SARS-CoV-2 pandemic, modern civilization is not immune to such events. Globalization and ease of travel have greatly increased the ability for viral outbreaks to spread around the world in a short period of time.

Understanding the molecular and immunological factors that bring about infection, cellular death, and long-term injury during Influenza infection will aid in the development of novel immunotherapies and/or vaccine candidates to reduce cardiac damage during future influenza infections. Ultimately, this research will give us a better understanding of the full spectrum of the pathogenesis of influenza and other viruses like it.


This project is currently seeking a funding partner. Please contact the JCVI Development Office at to learn more.

Principal Investigator


Matthew Frieman
University of Maryland

Peter Dube
University of Texas Health San Antonio

Related Research


This project is currently seeking a funding partner. Please contact the JCVI Development Office

Jill Mullen
Sr. Vice President of Philanthropy and Strategic Alliances