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    Poster Networking

    COVID

    Poster Networking Session

    PB0046 - Increased Platelet Activation demonstrated by Elevated CD36 and P-Selectin Expression in 1-year Post Recovered COVID-19 Patients

    Sunday, June 25, 2023
    18:30 – 19:30 ET
    Room: Exhibition

      Presenting Author(s)

    • Samuel SY Wang, Bmed, MD, PDipMDPath (he/him/his)

      Medical Officer
      Tan Tock Seng Hospital
      Singapore, Singapore

      • Co-Author(s)

    • KC

      Keefe Chee

      Scientist
      Beckon Dickinson, Singapore
      Singapore, Singapore

    • SW

      Shiun Woei Wong

      Doctor
      Department of Cardiology, Tan Tock Seng Hospital, Singapore
      Singapore, Singapore

    • GT

      Guat Bee Tan

      Scientist
      Department of Laboratory Medicine, Tan Tock Seng Hospital, Singapore
      Singapore, Singapore

    • HA

      Hong Ang

      Scientist
      Department of Laboratory Medicine, Tan Tock Seng Hospital, Singapore
      Singapore, Singapore

    • BL

      Bernard PuiLam Leung

      Scientist
      Yong Loo Lin School of Medicine, National University of Singapore, Singapore
      Singapore, Singapore

    • CT

      Chuen Wen Tan

      Doctor
      Department of Haematology, Singapore General Hospital Singapore
      Singapore, Singapore

    • KR

      Kollengode Ramanathan

      Doctor
      Department of Cardiothoracic and Vascular Surgery, National University Heart Centre, Singapore
      Singapore, Singapore

    • RD

      Rinkoo Dalan

      Doctor
      Department of Endocrinology, Tan Tock Seng Hospital, Singapore
      Singapore, Singapore

    • CC

      Christine Cheung

      Scientist
      Institute of Molecular and Cell Biology, A*STAR, Singapore
      Singapore, Singapore

    • DL

      David Chien Lye

      Doctor
      National Centre for Infectious Diseases, Singapore
      Singapore, Singapore

    • BY

      Barnaby Edward Young

      Doctor
      National Centre for Infectious Diseases, Singapore
      Singapore, Singapore

    • EY

      Eng Soo Yap

      Doctor
      Department of Haematology-Oncology, National University Health System, Singapore
      Singapore, Singapore

    • YC

      Yew Woon Chia

      Doctor
      Department of Cardiology, Tan Tock Seng Hospital, Singapore
      Singapore, Singapore

    • Bingwen Eugene Fan, MBBS, MRCP, MMED

      Consultant
      Department of Haematology, Tan Tock Seng Hospital, Singapore
      Singapore, Singapore

    Background: Hypercoagulability and platelet hyperactivity are characteristic of COVID-19 infection and contribute to an increased thrombotic burden. This clinical phenomenon was observed during acute illness and in post recovery period.

    Aims: We examined the platelet activation profile of patients up to 16 months post COVID-19 infection.

    Methods: Patients were divided into asymptomatic (n = 9), mild (n = 19) and classified as one group (n = 28). Moderate (4L oxygen) (n = 2), and severe (admitted to intensive care unit) (n = 6) were classified as a second group (n = 8). 17 healthy donors with no prior COVID-19 history served as controls. Whole blood was collected with acid citrate dextrose/sodium citrate vacutainer tubes for flow cytometry. A 10-color panel was designed with the following monoclonal antibodies: CD63,BV421,CD61,BV510,CD36,BV605,PAC-1FITC,GPVIPE,CD42a/PerCP,CD235a,PE-Cy7,CD62P APC,CD42b R718,CD45 APC-H7. The panel was prepared with Brilliant Stain Buffer and acquired on Becton Dickinson FACSCanto 10C. Flow Cytometry data was analysed using FlowJo 10.8.1, with Pairwise Controlled Manifold Approximation (PaCMAP) v1.0. Statistical analyses was done using ANOVA with Tukey’s multiple comparison method using GraphPad Prism 9.4.

    Results: Prior COVID-19 infection appeared to generate a subset of persistently activated CD62P+, PAC1+ and CD36+ platelets. This subset was observed in both asymptomatic/mild and moderate/severe patients (Figure 1A and Figure 1B). Further population gating confirmed dual expression of CD62P+/PAC1+. (Figure 1C). CD36 and CD62P levels were higher in patients with COVID-19 infection, with more severe disease associated with higher levels. (Figure 1D). We postulate that persistent platelet activation may be due to immune dysregulation and persistent inflammation triggered by COVID-19 infection. (Table 1)

    Conclusion(s): Our study provides early evidence for hyperactivated platelet phenotype in recovered COVID-19 patients, given their elevated CD62P and CD36 levels. This phenotype manifests more frequently in recovered survivors with severe infections. Further studies are needed to assess platelet activation/platelet exhaustion to confirm this postulate.