COVID-19 illness and autoimmune diseases: recent insights

Abstract

Background The aim of this review is to explore whether patients with autoimmune diseases (AIDs) were at high risk of infection during the COVID-19 epidemic and how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic affected immune system. Methods A systematic literature search was performed using the foreign databases (NCBI, web of science, EBSCO, ELSEVIER ScienceDirect) and Chinese databases (WanFang, CNKI (China National Knowledge Infrastructure), VIP, CBM) to locate all relevant publications (up to January 10, 2021). The search strategies used Medical Search Headings (MeSH) headings and keywords for “COVID-19” or “SARS-CoV-2” or “coronavirus” and “autoimmune disease”. Results This review evaluates the effect of SARS-CoV-2 on the immune system through ACE-2 receptor binding as the main pathway for cell attachment and invasion. It is speculated that SARS-COV-2 infection can activate lymphocytes and inflammatory response, which may play a role in the clinical onset of AIDs and also patients were treated with immunomodulatory drugs during COVID-19 outbreak. Preliminary studies suggested that the risk of developing severe forms of COVID-19 in patients with AIDs treated with immunomodulators or biologics might not increase. A large number of samples are needed for further verification, leading to an excessive immune response to external stimuli. Conclusion The relationship between autoimmune diseases and SARS-CoV-2 infection is complex. During the COVID-19 epidemic, individualized interventions for AIDs should be provided such as Internet-based service.

Pathogenic implications, incidence, and outcomes of COVID-19 in autoimmune inflammatory joint diseases and autoinflammatory disorders

“…During COVID-19, it has been shown that ACE2-expressing macrophages contained SARS-CoV-2 nucleoprotein antigen. These cells also showed an upregulation of IL-6, which may contribute to the excessive inflammatory burden and correlate with the disease severity [23]. Moreover, other proinflammatory chemokines and pro-inflammatory cytokines may be secreted by SARS-CoV-2-infected alveolar macrophages, which may further enhance the inflammation [23].…”

“…These cells also showed an upregulation of IL-6, which may contribute to the excessive inflammatory burden and correlate with the disease severity [23]. Moreover, other proinflammatory chemokines and pro-inflammatory cytokines may be secreted by SARS-CoV-2-infected alveolar macrophages, which may further enhance the inflammation [23]. Interestingly, during COVD-19, two chemokines (CCL2 and CCL7) resulted to be increased in the bronchoalveolar fluid [24].…”

“…In fact, in the pulmonary interstitium of SARS-CoV-infected patients, CD8+T cells are the most common infiltrative inflammatory cells, playing an important role in virus clearance as well as in immune-mediated injury [22]. In addition, SARS-CoV2 infection may activate lymphocytes and macrophage by the binding with angiotensin-converting enzyme 2 (ACE-2) receptor [23]. During COVID-19, it has been shown that ACE2-expressing macrophages contained SARS-CoV-2 nucleoprotein antigen.…”

SARS‐CoV‐2 infection does not seem to worsen the clinical course of patients with oral autoimmune disease

“…According to recent publication, patients diagnosed with systemic autoimmune diseases do not seem to carry an increased risk of COVID‐19 as compared to the general population (Emmi et al, 2020 ). Moreover, even if it has been speculated that SARS‐COV‐2 infection could activate lymphocytes and inflammatory response, preliminary studies suggested that the risk of developing severe forms of COVID‐19 in patients with AD, treated with immunomodulators or biologics, might not increase (Li et al, 2021 ).…”

Aminodihydrophthalazinedione sodium in prevention, therapy and rehabilitation of patients with respiratory diseases

“…Таким образом, иммунная система организма человека в борьбе с коронавирусом SARS-CoV-2 подвергается выраженным колебаниям и дисфункции в виде иммуносупрессии и активации явления аутоиммунитета [ 45,53,54].…”