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Severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) damages multiple organs, including the thyroid, by direct invasion and cell entry via angiotensin‐converting enzyme 2 or indirectly by promoting excessive inflammation in the body. The immune system is a critical factor in antiviral immunity and disease progression. In the context of SARS‐CoV‐2 infection, the immune system may become overly activated, resulting in a shift from regulatory to effector responses, which may subsequently promote the development and progression of autoimmune diseases. The incidence of autoimmune thyroid diseases, such as subacute thyroiditis, Graves' disease, and Hashimoto's thyroiditis, increases in individuals with COVID‐19 infection. This phenomenon may be attributed to aberrant responses of T‐cell subtypes, the presence of autoantibodies, impaired regulatory cell function, and excessive production of inflammatory cytokines, namely interleukin (IL)‐6, IL‐1β, interferon‐γ, and tumor necrosis factor‐α. Therefore, insights into the immune responses involved in the development of autoimmune thyroid disease according to COVID‐19 can help identify potential therapeutic approaches and guide the development of effective interventions to alleviate patients' symptoms. [ABSTRACT FROM AUTHOR]

Understanding the pathophysiology of long COVID is one of the most intriguing challenges confronting contemporary medicine. Despite observations recently made in the relevant molecular, cellular, and physiological domains, it is still difficult to say whether the post-acute sequelae of COVID-19 directly correspond to the consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This work hypothesizes that neutrophils and neutrophil extracellular traps (NETs) production are at the interconnection of three positive feedback loops which are initiated in the acute phase of SARS-CoV-2 infection, and which involve inflammation, immunothrombosis, and autoimmunity. This phenomenon could be favored by the fact that SARS-CoV-2 may directly bind and penetrate neutrophils. The ensuing strong neutrophil stimulation leads to a progressive amplification of an exacerbated and uncontrolled NETs production, potentially persisting for months beyond the acute phase of infection. This continuous self-stimulation of neutrophils leads, in turn, to systemic inflammation, micro-thromboses, and the production of autoantibodies, whose significant consequences include the persistence of endothelial and multiorgan damage, and vascular complications., (© 2024 The Author(s). Journal of Medical Virology published by Wiley Periodicals LLC.)

Here, we performed single-cell RNA sequencing of S1 and receptor binding domain protein-specific B cells from convalescent COVID-19 patients with different clinical manifestations. This study aimed to evaluate the role and developmental pathway of atypical memory B cells (MBCs) in response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The results revealed a proinflammatory signature across B cell subsets associated with disease severity, as evidenced by the upregulation of genes such as GADD45B, MAP3K8, and NFKBIA in critical and severe individuals. Furthermore, the analysis of atypical MBCs suggested a developmental pathway similar to that of conventional MBCs through germinal centers, as indicated by the expression of several genes involved in germinal center processes, including CXCR4, CXCR5, BCL2, and MYC. Additionally, the upregulation of genes characteristic of the immune response in COVID-19, such as ZFP36 and DUSP1, suggested that the differentiation and activation of atypical MBCs may be influenced by exposure to SARS-CoV-2 and that these genes may contribute to the immune response for COVID-19 recovery. Our study contributes to a better understanding of atypical MBCs in COVID-19 and the role of other B cell subsets across different clinical manifestations., (© 2024 The Author(s). Journal of Medical Virology published by Wiley Periodicals LLC.)

The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection is associated with increased levels of autoantibodies targeting immunological proteins such as cytokines and chemokines. Reports further indicate that COVID‐19 patients may develop a broad spectrum of autoimmune diseases due to reasons not fully understood. Even so, the landscape of autoantibodies induced by SARS‐CoV‐2 infection remains uncharted territory. To gain more insight, we carried out a comprehensive assessment of autoantibodies known to be linked to diverse autoimmune diseases observed in COVID‐19 patients in a cohort of 231 individuals, of which 161 were COVID‐19 patients (72 with mild, 61 moderate, and 28 with severe disease) and 70 were healthy controls. Dysregulated IgG and IgA autoantibody signatures, characterized mainly by elevated concentrations, occurred predominantly in patients with moderate or severe COVID‐19 infection. Autoantibody levels often accompanied anti‐SARS‐CoV‐2 antibody concentrations while stratifying COVID‐19 severity as indicated by random forest and principal component analyses. Furthermore, while young versus elderly COVID‐19 patients showed only slight differences in autoantibody levels, elderly patients with severe disease presented higher IgG autoantibody concentrations than young individuals with severe COVID‐19. This work maps the intersection of COVID‐19 and autoimmunity by demonstrating the dysregulation of multiple autoantibodies triggered during SARS‐CoV‐2 infection. Thus, this cross‐sectional study suggests that SARS‐CoV‐2 infection induces autoantibody signatures associated with COVID‐19 severity and several autoantibodies that can be used as biomarkers of COVID‐19 severity, indicating autoantibodies as potential therapeutical targets for these patients. [ABSTRACT FROM AUTHOR]

The precise interaction between the immune system and severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) is critical in deciphering the pathogenesis of coronavirus disease 2019 (COVID‐19) and is also vital for developing novel therapeutic tools, including monoclonal antibodies, antivirals drugs, and vaccines. Viral infections need innate and adaptive immune reactions since the various immune components, such as neutrophils, macrophages, CD4+ T, CD8+ T, and B lymphocytes, play different roles in various infections. Consequently, the characterization of innate and adaptive immune reactions toward SARS‐CoV‐2 is crucial for defining the pathogenicity of COVID‐19. In this study, we explain what is currently understood concerning the conventional immune reactions to SARS‐CoV‐2 infection to shed light on the protective and pathogenic role of immune response in this case. Also, in particular, we investigate the in‐depth roles of other immune mediators, including neutrophil elastase, serum amyloid A, and syndecan, in the immunopathogenesis of COVID‐19. [ABSTRACT FROM AUTHOR]