Department of Medicine, Division of Cardiovascular Medicine; Department of Medicine, Division of Infectious Disease and Immunology
Cardiology | Cardiovascular Diseases | Cells | Fluids and Secretions | Hemic and Immune Systems | Immunity | Immunology of Infectious Disease | Immunopathology | Infectious Disease | Influenza Humans | Respiratory Tract Diseases | Virus Diseases
Influenza infection increases the incidence of myocardial infarction but the reason is unknown. Platelets mediate vascular occlusion through thrombotic functions but are also recognized to have immunomodulatory activity. To determine if platelet processes are activated during influenza infection, we collected blood from 18 patients with acute influenza infection. Microscopy reveals activated platelets, many containing viral particles and extracellular-DNA associated with platelets. To understand the mechanism, we isolate human platelets and treat them with influenza A virus. Viral-engulfment leads to C3 release from platelets as a function of TLR7 and C3 leads to neutrophil-DNA release and aggregation. TLR7 specificity is confirmed in murine models lacking the receptor, and platelet depletion models support platelet-mediated C3 and neutrophil-DNA release post-influenza infection. These findings demonstrate that the initial intrinsic defense against influenza is mediated by platelet-neutrophil cross-communication that tightly regulates host immune and complement responses but can also lead to thrombotic vascular occlusion.
influenza, influenza infection, platelets, myocardial infarction
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DOI of Published Version
Nat Commun. 2019 Apr 16;10(1):1780. doi: 10.1038/s41467-019-09607-x. Link to article on publisher's site
Koupenova-Zamor M, Corkrey HA, Vitseva O, Manni G, Pang CJ, Clancy L, Yao C, Rade JJ, Levy D, Wang JP, Finberg RW, Kurt-Jones EA, Freedman JE. (2019). The role of platelets in mediating a response to human influenza infection. Open Access Articles. https://doi.org/10.1038/s41467-019-09607-x. Retrieved from https://escholarship.umassmed.edu/oapubs/3836
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This work is licensed under a Creative Commons Attribution 4.0 License.
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