Influenza-induced thrombocytopenia is dependent on the subtype and sialoglycan receptor and increases with virus pathogenicity

A.J. Gerard Jansen, Thom Spaan, Hui Zhi Low, Daniele Di Iorio, Judith van den Brand, Malte Tieke, Arjan Barendrecht, Kerstin Rohn, Geert van Amerongen, Koert Stittelaar, Wolfgang Baumgärtner, Albert Osterhaus, Thijs Kuiken, Geert Jan Boons, Jurriaan Huskens, Marianne Boes, Coen Maas, Erhard van der Vries*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

47 Citations (Scopus)
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Thrombocytopenia is a common complication of influenza virus infection, and its severity predicts the clinical outcome of critically ill patients. The underlying cause(s) remain incompletely understood. In this study, in patients with an influenza A/H1N1 virus infection, viral load and platelet count correlated inversely during the acute infection phase. We confirmed this finding in a ferret model of influenza virus infection. In these animals, platelet count decreased with the degree of virus pathogenicity varying from 0% in animals infected with the influenza A/H3N2 virus, to 22% in those with the pandemic influenza A/H1N1 virus, upto62%in animals with a highly pathogenic A/H5N1 virus infection. This thrombocytopenia is associated with virus-containing platelets that circulate in the blood. Uptake of influenza virus particles by platelets requires binding to sialoglycans and results in the removal of sialic acids by the virus neuraminidase, a trigger for hepatic clearance of platelets. We propose the clearance of influenza virus by platelets as a paradigm. These insights clarify the pathophysiology of influenza virus infection and show how severe respiratory infections, including COVID-19, may propagate thrombocytopenia and/or thromboembolic complications.

Original languageEnglish
Pages (from-to)2967-2978
Number of pages12
JournalBlood advances
Issue number13
Publication statusPublished - 14 Jul 2020


  • Degree of thrombocytopenia and platelet activation is dependent on the influenza virus subtype and may contribute to virus pathogenicity
  • Key points
  • Platelets and influenza virus interact in a sialic acid-dependent manner
  • Which may designate platelets for hepatic clearance.
  • 22/2 OA procedure


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