Risk surveillance and mitigation: autoantibodies as triggers and inhibitors of severe reactions to SARS-CoV-2 infection

COVID-19 clinical presentation differs considerably between individuals, ranging from asymptomatic, mild/moderate and severe disease which in some cases are fatal or result in long-term effects. Identifying immune mechanisms behind severe disease development informs screening strategies to predict who are at greater risk of developing life-threatening complications. However, to date clear prognostic indicators of individual risk of severe or long COVID remain elusive. Autoantibodies recognize a range of self-antigens and upon antigen recognition and binding, important processes involved in inflammation, pathogen defence and coagulation are modified. Recent studies report a significantly higher prevalence of autoantibodies that target immunomodulatory proteins including cytokines, chemokines, complement components, and cell surface proteins in COVID-19 patients experiencing severe disease compared to those who experience mild or asymptomatic infections. Here we discuss the diverse impacts of autoantibodies on immune processes and associations with severe COVID-19 disease.

Automated summary

The clinical presentation of COVID-19 varies significantly between individuals, from asymptomatic, mild/moderate to severe disease. Understanding the immune mechanisms behind severe disease can help predict life-threatening complications, with autoantibodies playing a crucial role in inflammation, pathogen defense, and coagulation processes. Studies show a higher prevalence of autoantibodies targeting immunomodulatory proteins in severe COVID-19 patients compared to those with mild or asymptomatic infections.