西奈山伊坎医学院Filip K. Swirski小组的一项最新研究认为流感劫持骨髓细胞，在心脏造成I型干扰素引发的损伤。相关论文发表在2026年2月9日出版的《免疫学》杂志上。

该研究组发现流感感染损害了人类和小鼠的心脏。在小鼠中，该课题组发现在肺部感染后不久，病毒感染了表达高浓度趋化因子受体CCR2的循环髓系前树突状细胞3（前DC3）。产生大量CCL2的心脏优先吸引被感染的原DC3。在心肌中，病毒逃离原DC3，感染心肌细胞，并触发i型干扰素（IFN-I）的产生。IFN-I受体（IFNAR1）参与心肌细胞的组织损伤和心功能受损。基因和治疗上抑制IFNAR1仅在心肌细胞中保护心脏，同时保持肺的抗病毒免疫。他们的研究结果确定了一系列宿主-病原体相互作用，这些相互作用会传播组织损伤，并揭示了一种干预轴，以减轻病毒感染后的心血管风险。

研究人员表示，大量证据表明流感感染与心血管疾病相关，但将感染与心脏联系起来的机制仍然知之甚少。

附：英文原文

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

Author: Jeffrey Downey, Ana Oliveira-Coelho, Máté G. Kiss, Gabriel Laghlali, Alexander Leunig, Emir Radkevich, Laszlo Halasz, Martin Umali, Joana Ferreira da Silva, Madeline L. Eller, Matteo Gianeselli, Magdalena M. ak, Haley E. Randolph, Gabriel Caumartin, Wolfram C. Poller, Henrike Janssen, Laura L. Koekkoek, Jamshid Abdul-Ghafar, Pacific Huynh, Darwin D’Souza, Vladimir Roudko, Sheqouia Nauta, Jazz Munitz, Xisheng Li, Thomas Rathner, Ziche Chen, Anh Phan, Abigail Glick, Katarzyna Cialowicz, Zhihong Chen, Seunghee Kim-Schulze, Seonghun Yoon, Matthias Nahrendorf, Susmita Sahoo, Miriam Merad, Adolfo García-Sastre, Cameron S. McAlpine, Gustav J. Strijkers, Viviana Simon, Rachel Brody, Saurabh Mehandru, Zahi A. Fayad, Benjamin P. Kleinstiver, Lior Zangi, Mandy M.T. van Leent, Michael Schotsaert, Filip K. Swirski

Issue&Volume: 2026-02-09

Abstract: Abundant evidence has correlated influenza infection with cardiovascular disease, yet mechanisms linking infection with the heart remain poorly understood. Here, we show that influenza infection damaged the human and murine heart. In mice, we showed that shortly after pulmonary infection, the virus infected a circulating myeloid pro-dendritic cell 3 (pro-DC3) that expressed high concentrations of the chemokine receptor CCR2. The heart, which produces abundant CCL2, preferentially attracted infected pro-DC3. In the myocardium, the virus escaped pro-DC3, infected cardiomyocytes, and triggered production of type-I interferon (IFN-I). Engagement of the IFN-I receptor (IFNAR1) on cardiomyocytes caused tissue damage and compromised heart function. Genetically and therapeutically dampening IFNAR1 exclusively in cardiomyocytes protected the heart while preserving anti-viral immunity in the lung. Our results identify a series of host-pathogen interactions that propagate tissue damage and uncover an axis for intervention to mitigate cardiovascular risk following viral infection.

DOI: 10.1016/j.immuni.2025.12.011

Source: https://www.cell.com/immunity/abstract/S1074-7613(25)00567-9