Background Several studies suggested that SARS-CoV-2 infection may induce autoantibodies related to autoimmune rheumatic diseases (ARD).

Objectives To determine whether polyclonal antibodies from SARS-CoV-2 uninfected patients with ARDs cross-react with SARS-CoV-2 and vice versa.

Methods 90 sera positive at high-titres for 23 common autoantibodies (all sera stored before 2018), were tested for reactivity against proteins of SARS-CoV-2 (spike protein S1, nucleocapsid NC etc) by ELISA and CMIA. Vice versa, 10 monoclonal antibodies against S1 protein (most of them against RBD) were tested for autoantibody reactivity by indirect immunofluorescence, ELISA, immunoblot and dot/line immunoassays coated with different antigens. Ten post-COVID sera with high titers of anti-Spike abs were tested by ELISAs for reactivity against various autoantigens related to ARDs.

Results 88 out of 90 samples (%), were totally unreactive to SARS-CoV-2 proteins; 2 sera, one anti-CCP and one anti-CENP reacted against S protein. All sera tested negative for neutralized abs against SARS-CoV-2. None of 10 sera from SARS-CoV-2 infected patients reacted with different autoantigens by molecular assays. None of the 10 monoclonal abs against S1 protein reacted with 23 different self-antigens. On HEp2 cells as substrate for IIF, 3 of the 10 monoclonal abs gave a low-titre coarse speckled pattern. No reactivity was found by IIFL using tissue substrates.

Conclusion Our data do not suggest a dominant role for molecular mimicry and immunological cross reactivity as a trigger of autoantibodies related to ARDs.

Disclosure of Interests Christos Liaskos: None declared, Eleni Patrikiou: None declared, Lars Komorowski Employee of: emploee of EUROIMMUN Medizinische Labordiagnostika, Christina Tsigalou: None declared, Alexandra Tsirogianni: None declared, Lazaros Sakkas: None declared, Dimitrios Bogdanos: None declared