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LIBORIO CAVALERI

Genetic justification of severe COVID-19 using a rigorous algorithm

  • Autori: Gavriilaki E.; Asteris P.G.; Touloumenidou T.; Koravou E.-E.; Koutra M.; Papayanni P.G.; Karali V.; Papalexandri A.; Varelas C.; Chatzopoulou F.; Chatzidimitriou M.; Chatzidimitriou D.; Veleni A.; Grigoriadis S.; Rapti E.; Chloros D.; Kioumis I.; Kaimakamis E.; Bitzani M.; Boumpas D.; Tsantes A.; Sotiropoulos D.; Sakellari I.; Kalantzis I.G.; Parastatidis S.T.; Koopialipoor M.; Cavaleri L.; Armaghani D.J.; Papadopoulou A.; Brodsky R.A.; Kokoris S.; Anagnostopoulos A.
  • Anno di pubblicazione: 2021
  • Tipologia: Articolo in rivista
  • Parole Chiave: Complement Activation; Complement C3
  • OA Link: http://hdl.handle.net/10447/519787

Abstract

Recent studies suggest excessive complement activation in severe coronavirus disease-19 (COVID-19). The latter shares common characteristics with complement-mediated thrombotic microangiopathy (TMA). We hypothesized that genetic susceptibility would be evident in patients with severe COVID-19 (similar to TMA) and associated with disease severity. We analyzed genetic and clinical data from 97 patients hospitalized for COVID-19. Through targeted next-generation-sequencing we found an ADAMTS13 variant in 49 patients, along with two risk factor variants (C3, 21 patients; CFH,34 patients). 31 (32%) patients had a combination of these, which was independently associated with ICU hospitalization (p = 0.022). Analysis of almost infinite variant combinations showed that patients with rs1042580 in thrombomodulin and without rs800292 in complement factor H did not require ICU hospitalization. We also observed gender differences in ADAMTS13 and complement-related variants. In light of encouraging results by complement inhibitors, our study highlights a patient population that might benefit from early initiation of specific treatment.