tetano
Editor, Senior Moderator
PLoS Pathog
. 2021 Dec 3;17(12):e1010118.
doi: 10.1371/journal.ppat.1010118. Online ahead of print.
Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
Marc Emmenegger[SUP] 1 [/SUP], Sreedhar Saseendran Kumar[SUP] 2 [/SUP], Vishalini Emmenegger[SUP] 2 [/SUP], Tomas Malinauskas[SUP] 3 [/SUP], Thomas Buettner[SUP] 4 [/SUP], Laura Rose[SUP] 4 [/SUP], Peter Schierack[SUP] 5 6 [/SUP], Martin F Sprinzl[SUP] 7 8 [/SUP], Clemens J Sommer[SUP] 9 [/SUP], Karl J Lackner[SUP] 8 [/SUP], Adriano Aguzzi[SUP] 1 [/SUP], Dirk Roggenbuck[SUP] 4 5 6 [/SUP], Katrin B M Frauenknecht[SUP] 1 9 [/SUP]
Affiliations
Abstract
Antiphospholipid antibodies (aPL), assumed to cause antiphospholipid syndrome (APS), are notorious for their heterogeneity in targeting phospholipids and phospholipid-binding proteins. The persistent presence of Lupus anticoagulant and/or aPL against cardiolipin and/or β2 glycoprotein I have been shown to be independent risk factors for vascular thrombosis and pregnancy morbidity in APS. aPL production is thought to be triggered by-among other factors-viral infections, though infection-associated aPL have mostly been considered non-pathogenic. Recently, the potential pathogenicity of infection-associated aPL has gained momentum since an increasing number of patients infected with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been described with coagulation abnormalities and hyperinflammation, together with the presence of aPL. Here, we present data from a multicentric, mixed-severity study including three cohorts of individuals who contracted SARS-CoV-2 as well as non-infected blood donors. We simultaneously measured 10 different criteria and non-criteria aPL (IgM and IgG) by using a line immunoassay. Further, IgG antibody response against three SARS-CoV-2 proteins was investigated using tripartite automated blood immunoassay technology. Our analyses revealed that selected non-criteria aPL were enriched concomitant to or after an infection with SARS-CoV-2. Linear mixed-effects models suggest an association of aPL with prothrombin (PT). The strength of the antibody response against SARS-CoV-2 was further influenced by SARS-CoV-2 disease severity and sex of the individuals. In conclusion, our study is the first to report an association between disease severity, anti-SARS-CoV-2 immunoreactivity, and aPL against PT in patients with SARS-CoV-2.
. 2021 Dec 3;17(12):e1010118.
doi: 10.1371/journal.ppat.1010118. Online ahead of print.
Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
Marc Emmenegger[SUP] 1 [/SUP], Sreedhar Saseendran Kumar[SUP] 2 [/SUP], Vishalini Emmenegger[SUP] 2 [/SUP], Tomas Malinauskas[SUP] 3 [/SUP], Thomas Buettner[SUP] 4 [/SUP], Laura Rose[SUP] 4 [/SUP], Peter Schierack[SUP] 5 6 [/SUP], Martin F Sprinzl[SUP] 7 8 [/SUP], Clemens J Sommer[SUP] 9 [/SUP], Karl J Lackner[SUP] 8 [/SUP], Adriano Aguzzi[SUP] 1 [/SUP], Dirk Roggenbuck[SUP] 4 5 6 [/SUP], Katrin B M Frauenknecht[SUP] 1 9 [/SUP]
Affiliations
- PMID: 34860860
- DOI: 10.1371/journal.ppat.1010118
Abstract
Antiphospholipid antibodies (aPL), assumed to cause antiphospholipid syndrome (APS), are notorious for their heterogeneity in targeting phospholipids and phospholipid-binding proteins. The persistent presence of Lupus anticoagulant and/or aPL against cardiolipin and/or β2 glycoprotein I have been shown to be independent risk factors for vascular thrombosis and pregnancy morbidity in APS. aPL production is thought to be triggered by-among other factors-viral infections, though infection-associated aPL have mostly been considered non-pathogenic. Recently, the potential pathogenicity of infection-associated aPL has gained momentum since an increasing number of patients infected with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been described with coagulation abnormalities and hyperinflammation, together with the presence of aPL. Here, we present data from a multicentric, mixed-severity study including three cohorts of individuals who contracted SARS-CoV-2 as well as non-infected blood donors. We simultaneously measured 10 different criteria and non-criteria aPL (IgM and IgG) by using a line immunoassay. Further, IgG antibody response against three SARS-CoV-2 proteins was investigated using tripartite automated blood immunoassay technology. Our analyses revealed that selected non-criteria aPL were enriched concomitant to or after an infection with SARS-CoV-2. Linear mixed-effects models suggest an association of aPL with prothrombin (PT). The strength of the antibody response against SARS-CoV-2 was further influenced by SARS-CoV-2 disease severity and sex of the individuals. In conclusion, our study is the first to report an association between disease severity, anti-SARS-CoV-2 immunoreactivity, and aPL against PT in patients with SARS-CoV-2.