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. 2023 Jan;95(1):e28273.
doi: 10.1002/jmv.28273. Epub 2022 Nov 11.

IgG autoantibodies against ACE2 in SARS-CoV-2 infected patients

Affiliations

IgG autoantibodies against ACE2 in SARS-CoV-2 infected patients

Ewelina Hallmann et al. J Med Virol. 2023 Jan.

Abstract

How frequently autoantibodies against angiotensin-converting enzyme 2 (ACE2) occur in patients infected by SARS-CoV-2 is understudied and limited to investigations on a small sample size. The presence of these antibodies may contribute to the long-lasting effects of COVID-19 observed in some individuals, particularly if IgG-class antibodies would emerge in patients. This study assessed the prevalence of IgG autoantibodies against ACE2 in 1139 patients infected with SARS-CoV-2 and examined their relationship with severity, demographic characteristics, and status of vaccination against influenza. The overall prevalence of anti-ACE IgG antibodies in our cohort was 1.5%. Most of these individuals were men (76.5%) and underwent mild COVID-19, but some severe and asymptomatic cases were also observed. Patients with severe infection had twofold higher titers than mild and asymptomatic cases. Age, comorbidities, and influenza vaccination status were not related to antibody prevalence. The prevalence of IgG anti-SARS-CoV-2 antibodies (against nucleocapsid protein and S2 subunit, but not against receptor-binding domain) was higher in the subset with ACE2 autoantibodies. Further research is required to understand the potential spectrum and duration of effects of IgG autoantibodies against ACE2 in patients after SARS-CoV-2 infection, particularly concerning long COVID-19.

Keywords: COVID-19; autoantibody; autoimmunity; renin-angiotensin system.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
(A) Distribution of patients with IgG autoantibodies against ACE2 (n = 17) in relation to the severity of SARS‐CoV‐2 infection. (B) Titers of IgG autoantibodies against ACE2 I in relation to the severity of SARS‐CoV‐2 infection.

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