PropertyValue
?:abstract
  • There is an urgent need to understand the underlying mechanisms contributing to thrombotic and inflammatory complications during COVID-19. Data from independent groups have identified that platelets are hyperreactive during COVID-19. Platelet hyperreactivity is accompanied by changes in platelet gene expression, and enhanced interactions between platelets and leukocytes. In some patients, SARS-CoV-2 mRNA has been detected in platelets. Together, this suggests that SARS-CoV-2 may interact with platelets. However, controversy remains on which receptors mediate SARS-CoV-2 platelet interactions. Most, but not all, transcriptomic and proteomic analyses fail to observe the putative SARS-CoV-2 receptor, angiotensin converting enzyme-2, or the cellular serine protease necessary for viral entry, TMPRSS2, on platelets and megakaryocytes. Interestingly, platelets express other known SARS-CoV-2 receptors, which induce similar patterns of activation to those observed when platelets are incubated with SARS-CoV-2. This Forum Article explores these findings, and discusses ongoing areas of controversy and uncertainty with regards to SARS-CoV-2 platelet interactions.
is ?:annotates of
?:creator
?:doi
?:doi
  • 10.1111/jth.15156
?:journal
  • Journal_of_thrombosis_and_haemostasis_:_JTH
?:license
  • unk
?:pmid
?:pmid
  • 33119197.0
?:publication_isRelatedTo_Disease
is ?:relation_isRelatedTo_publication of
?:source
  • Medline
?:title
  • Is there a role for the ACE2 receptor in SARS-CoV-2 interactions with platelets?
?:type
?:year
  • 2020-10-29

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