Cardiomyocytes recruit monocytes upon SARS-CoV-2 infection by secreting CCL2

Liuliu Yang, Benjamin E. Nilsson-Payant, Yuling Han, Fabrice Jaffré, Jiajun Zhu, Pengfei Wang, Tuo Zhang, David Redmond, Sean Houghton, Rasmus Møller, Daisy Hoagland, Lucia Carrau, Shu Horiuchi, Marisa Goff, Jean K. Lim, Yaron Bram, Chanel Richardson, Vasuretha Chandar, Alain Borczuk, Yaoxing HuangJenny Xiang, David D. Ho, Robert E. Schwartz, Benjamin R. tenOever, Todd Evans, Shuibing Chen

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology remains unknown. Here, using an established in vivo hamster model, we demonstrate that SARS-CoV-2 can be detected in cardiomyocytes of infected animals. Furthermore, we found damaged cardiomyocytes in hamsters and COVID-19 autopsy samples. To explore the mechanism, we show that both human pluripotent stem cell-derived cardiomyocytes (hPSC-derived CMs) and adult cardiomyocytes (CMs) can be productively infected by SARS-CoV-2, leading to secretion of the monocyte chemoattractant cytokine CCL2 and subsequent monocyte recruitment. Increased CCL2 expression and monocyte infiltration was also observed in the hearts of infected hamsters. Although infected CMs suffer damage, we find that the presence of macrophages significantly reduces SARS-CoV-2-infected CMs. Overall, our study provides direct evidence that SARS-CoV-2 infects CMs in vivo and suggests a mechanism of immune cell infiltration and histopathology in heart tissues of COVID-19 patients.

Original languageEnglish
Pages (from-to)2274-2288
Number of pages15
JournalStem Cell Reports
Issue number9
StatePublished - 14 Sep 2021


  • CCL2
  • COVID-19
  • cardiomyocyte
  • hPSC
  • hamster
  • immune cell infiltration


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