Patients with severe COVID-19 do not have elevated autoantibodies against common diagnostic autoantigens

Abstract

Objectives Infection by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the causative pathogen of coronavirus disease 2019 (COVID-19) presents occasionally with an aberrant autoinflammatory response, including the presence of elevated circulating autoantibodies in some individuals. Whether the development of autoantibodies against self-antigens affects COVID-19 outcomes remains unclear. To better understand the prognostic role of autoantibodies in COVID-19, we quantified autoantibodies against 23 markers that are used for diagnosis of autoimmune disease. To this end, we used serum samples from patients with severe [intensive care unit (ICU)] and moderate (ward) COVID-19, across two to six consecutive time points, and compared autoantibody levels to uninfected healthy and ICU controls. Methods Acute and post-acute serum (from 1 to 26 ICU days) was collected from 18 ICU COVID-19-positive patients at three to six time points; 18 ICU COVID-19-negative patients (sampled on ICU day 1 and 3); 21 ward COVID-19-positive patients (sampled on hospital day 1 and 3); and from 59 healthy uninfected controls deriving from two cohorts. Levels of IgG autoantibodies against 23 autoantigens, commonly used for autoimmune disease diagnosis, were measured in serum samples using MSD® U-PLEX electrochemiluminescence technology (MSD division Meso Scale Discovery®), and results were compared between groups. Results There were no significant elevations of autoantibodies for any of the markers tested in patients with severe COVID-19. Conclusions Sample collections at longer time points should be considered in future studies, for assessing the possible development of autoantibody responses following infection with SARS-CoV-2.

Knowledge mapping of COVID-19 and autoimmune diseases: a visual and bibliometric analysis

“…The presence of autoantibodies may predict the adverse clinical course of COVID-19 patients [ 59 ]. However, some studies have also indicated that autoantibodies to any marker tested were not significantly elevated in patients with severe COVID-19, such as anti-IFN antibodies that are unlikely to promote long-term COVID-19 symptoms after the acute phase of infection [ 60 , 61 ]. As for molecular mimicry, it is one of the mechanisms by which a virus can induce an autoimmune response, with the production of specific autoantibodies and the action of certain vaccine adjuvants seem to be important factors in the autoimmune phenomenon [ 53 , 62 ].…”

Effect of serum autoantibodies on the COVID-19 patient’s prognosis

“…Genetic susceptibility and hyperactivation of the host immune system may trigger autoimmune diseases (Esmaeili et al, 2017;Scappaticcio et al, 2021). Similar to patients infected with other viruses, infected with SARS-CoV-2 show altered autoantibody profiles (Zhou Y. et al, 2020;Peker et al, 2021;Scappaticcio et al, 2021b), such as, antinuclear antibodies, antithyroid antibodies, chromatin proteins, ribosomal proteins, and immunerelated proteins (Bastard et al, 2020;Chang et al, 2021;Ulndreaj et al, 2022). These autoantibodies are closely correlated with the disease severity and the prognosis of COVID-19 patients and may trigger long-COVID-19 symptoms (Pascolini et al, 2021;Stjepanovic et al, 2022;Son et al, 2023).…”

Antinuclear antibodies in individuals with COVID-19 reflect underlying disease: Identification of new autoantibodies in systemic sclerosis (CDK9) and malignancy (RNF20, RCC1, TRIP13)

“…Conversely, studies that evaluated clinically significant antibodies associated with systemic rheumatic diseases (e.g. dsDNA, centromere, chromatin, ribosomal P, SSA-, SS-B, Sm, RNP, Scl-70, Jo-1) concluded that acute COVID-19 is not associated with a high prevalence of such autoantibodies [ [8] , [9] , [10] ]. Generally, studies on ANA in COVID-19 were small with differences in reported antibody levels and prevalence across studies without in-depth analysis of the nature of the autoantigens.…”