Understanding immunopathological fallout of human coronavirus infections including COVID‐19: Will they cross the path of rheumatologists?

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causing coronavirus disease 2019 (COVID-19) is the biggest pandemic of our lifetime to date. No effective treatment is yet in sight for this catastrophic illness. Several antiviral agents and vaccines are in clinical trials, and drug repurposings as immediate and alternative choices are also under consideration. Immunomodulatory agents like hydroxychloroquine (HCQ) as well as biological disease-modifying anti-rheumatic drugs (bDMARDs) such as tocilizumab and anakinra received worldwide attention for treatment of critical patients with COVID-19. This is of interest to rheumatologists, who are well versed with rational use of these agents. This brief review addresses the understandings of some of the common immunopathogenetic mechanisms in the context of autoimmune rheumatic diseases like systemic lupus erythematosus (SLE) and COVID-19. Apart from demographic comparisons, the role of type I interferons (IFN), presence of antiphospholipid antibodies and finally mechanism of action of HCQ in both the scenarios are discussed here. High risks for fatal disease in COVID-19 include older age, metabolic syndrome, male gender, and individuals who develop delayed type I IFN response. HCQ acts by different mechanisms including prevention of cellular entry of SARS-CoV-2 and inhibition of type I IFN signaling. Recent controversies regarding efficacy of HCQ in management of COVID-19 warrant more studies in that direction. Autoantibodies were also reported in severe acute respiratory syndrome (SARS) as well as in COVID-19. Rheumatologists need to wait and see whether SARS-CoV-2 infection triggers development of autoimmunity in patients with COVID-19 infection in the long run.

Low levels of vitamin D were associated with coagulopathy among hospitalized coronavirus disease-19 (COVID-19) patients: A single-centered study in Indonesia

“…A previous study also showed that this novel coronavirus could also induce secondary anti-phospholipid syndrome (APS) by promoting the production of anti-phospholipid antibodies (APL-Abs) (9). Xiao et al (10) also support this study, which found that 47% of patients with COVID-19 in the intensive unit were positive for APL-Abs. However, it is still unclear whether these antibodies are associated with thrombosis in these patients.…”

Circulating Type I Interferon Levels and COVID-19 Severity: A Systematic Review and Meta-Analysis

“…The average incubation period is 5 days ( 3 ), and the most prevalent signs and symptoms are fever, cough, headache, myalgia, fatigue, gastrointestinal symptoms, and dyspnea ( 4 , 5 ). COVID-19 causes distinct clinical manifestations among affected individuals, ranging from asymptomatic cases to cases with mild, moderate, severe, or critical symptoms, where they might progress to an acute respiratory distress syndrome (SARS) or even to dysfunction of multiple organs, complications that lead to death ( 6 , 7 ). The risk of developing a more aggressive disease condition is influenced by age and the presence of comorbidities, such as diabetes, hypertension, obesity, and cardiovascular diseases ( 2 , 8 ).…”

Cutaneous lupus‐erythematosus‐like reaction arising after COVID‐19 vaccination

“…3 We theorize that these statistics are related to women having increased rates of autoimmunity and drug reactions in general. 5 There is reported overlap in the immune response that occurs during COVID-19 infection, after the RNA-based COVID-19 vaccines, and in the autoimmunity of systemic lupus erythematosus (SLE), including its cutaneous manifestations. 5,6 All produce an immune response with increased production of type I interferon (IFN) by plasmacytoid dendritic cells.…”