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Influenza hijacks myeloid cells to inflict type-I interferon-fueled damage in the heart

Jeffrey Downey1, Ana Oliveira-Coelho1, Máté G Kiss1

  • 1Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Immunity
|February 10, 2026
PubMed

Insights

Influenza infection damages the heart by infecting myeloid cells that carry the virus to the heart. Blocking the type-I interferon (IFN-I) receptor in heart cells protects against this cardiovascular damage.

Area of Science:

  • Cardiovascular Science
  • Infectious Disease Immunology
  • Virology

Background:

  • Influenza infection is linked to cardiovascular disease, but the underlying mechanisms are unclear.
  • Understanding how viral infections impact the heart is crucial for public health.
  • Existing research lacks detailed insights into the cardiac complications of influenza.

Purpose of the Study:

  • To elucidate the mechanisms by which influenza infection damages the heart.
  • To identify specific cellular interactions and molecular pathways involved in cardiac injury post-influenza.
  • To explore potential therapeutic targets for mitigating influenza-induced cardiovascular complications.

Main Methods:

  • Utilized murine models of influenza infection.
  • Tracked viral spread and cellular tropism following pulmonary infection.
  • Investigated the role of myeloid pro-dendritic cells (pro-DC3), chemokine receptors (CCR2, CCL2), and type-I interferon (IFN-I) signaling.
  • Assessed cardiac function and tissue damage.
  • Employed genetic and therapeutic strategies to modulate IFN-I receptor (IFNAR1) signaling in cardiomyocytes.

Main Results:

  • Influenza infection was shown to damage both human and murine hearts.
  • Pulmonary influenza infection led to the infection of circulating myeloid pro-DC3 cells expressing CCR2.
  • These infected cells were preferentially attracted to the heart due to CCL2 production.
  • The virus escaped pro-DC3 cells in the myocardium, infected cardiomyocytes, and induced IFN-I production.
  • IFNAR1 engagement on cardiomyocytes resulted in cardiac tissue damage and functional impairment.
  • Targeting IFNAR1 specifically in cardiomyocytes protected the heart without compromising lung antiviral immunity.

Conclusions:

  • Influenza infection propagates cardiac damage through a sequence of host-pathogen interactions.
  • Infected myeloid cells act as vectors, delivering the virus to the heart.
  • Type-I interferon signaling in cardiomyocytes is a key driver of cardiac dysfunction.
  • Targeting the IFNAR1 axis in cardiomyocytes offers a promising strategy to prevent cardiovascular complications of influenza.
Keywords:
cardiovascular diseaseheartinfluenzamyeloid cellspro-DC3type I interferon

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