Thrombosis after SARS-CoV2 infection or COVID-19 vaccination: will a nonpathologic anti-PF4 antibody be a solution?—A narrative review. Issue 3 (29th August 2022)

• Record Type: Journal Article
• Authors: Rao, Elizabeth; Grover, Payal; Zhang, Hongtao
• Is Part Of: Journal of bio-X research. Volume 5:Issue 3(2022)
• Page Start: 97
• Page End: 103
• Publication Date: 2022-08-29
• Subjects: antibody -- coagulation dysfunctions -- COVID-19 -- PF4 -- vaccine-induced immunological thrombotic thrombocytopenia; Biology -- Research -- Periodicals; Medicine -- Research -- Periodicals; Medicine -- Research; Biology -- Research; Biological Science Disciplines; Biomedical Research; Electronic journal; Periodicals; Electronic journals; Periodical; 570.724
• DOI: 10.1097/JBR.0000000000000125
• Languages: English
• ISSNs: 2096-5672

Abstract

Abstract : The coronavirus disease 2019 (COVID-19) pandemic was triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a previously unknown strain of coronavirus. To fully understand the consequences and complications of SARS-CoV-2 infections, we have reviewed current literature on coagulation dysfunctions that are related to the disease and vaccination. While COVID-19 is more commonly considered as a respiratory illness, studies indicate that, in addition to respiratory illness, a coagulation dysfunction may develop in individuals after the initial infection, placing them at the risk of developing thrombotic events. Patients who died of COVID-19 had higher levels of D-dimer, a biomarker for blood clot formation and breakdown. Effective treatments for coagulation dysfunctions are critically needed to improve patient survival. On the other hand, antibodies against platelet factor 4 (PF4)/heparin may be found in patients with rare instances of vaccine-induced immunological thrombotic thrombocytopenia (VITT) following vaccination with adenovirus-based vaccines. VITT is characterized by atypical thrombosis and thrombocytopenia, similar to immune-mediated heparin-induced thrombocytopenia (HIT), but with no need for heparin to trigger the immune response. Although both adenovirus-based and mRNA-based vaccines express the Spike protein of SARS-CoV-2, VITT is exclusively related to adenovirus-based vaccines. Due to the resemblance with HIT, the use of heparin is highly discouraged against treating patients with thrombotic thrombocytopenia after SARS-CoV-2 infection or with VITT after vaccination. Intravenous immunoglobulin therapy coupled with anticoagulation is recommended instead. The well-studied anti-PF4 monoclonal antibody RTO, which does not induce pathologic immune complexes in the presence of heparin and has been humanized for a potential treatment modality for HIT, may provide a nonanticoagulant HIT-specific solution to the problem of increased blood coagulation after SARS-CoV-2 infection or the VITT after immunization.