FIGURE 1.

Possible mechanism(s) for SARS‐CoV‐2 interactions with platelets. A subset of platelets from COVID‐19 patients contain SARS‐CoV‐2 mRNA. Angiotensin converting enzyme‐2 (ACE2) and TMPRSS2 are the primary mechanism for entry of SARS‐CoV‐2 into cells, but the expression of these proteins on platelets remains controversial. Manne et al⁹and Zaid et al¹³recently observed the absence of both proteins in platelets based on RNA‐seq, real‐time polymerase chain reaction analysis, and proteomic approaches.9., 13.In contrast, Zhang et al¹²demonstrated expression of both ACE and TMPRSS2 on platelets.¹²It remains possible that SARS‐CoV‐2 may use ACE2‐independent binding partners to interact with platelets, including CD147 and CD26. Extracellular vesicles containing SARS‐CoV‐2 released from infected endothelial cells may also interact with platelets, therefore allowing interactions and viral cellular entry independent of direct virus binding