Is there a link between COVID-19 and the risk of developing autoimmune diseases?

In a recent article published in nature review rheumatology News and Perspectives Researchers reviewed data on the incidence of autoimmune diseases in the post-acute coronavirus disease 2019 (COVID-19) period.

study: High risk of autoimmune disease after COVID-19. Image Credit: KaterynaKon/Shutterstock.com

Background

COVID-19 is causing unprecedented morbidity and mortality worldwide. The immunoprotection conferred by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine and previous COVID-19 history, combined with the development of effective therapeutic agents, has reduced COVID-19-related mortality. lowered.

However, post-COVID-19 conditions continue to increase, especially with new-onset autoimmune diseases during COVID-19 convalescence. Autoimmune diseases have been reported among adults following COVID-19. However, the prevalence and magnitude of disease and risk of occurrence in individuals infected with SARS-CoV-2 compared with uninfected individuals are not well characterized.

A better understanding of the impact of COVID-19 on the risk of developing acute complications of COVID-19, such as autoimmune diseases, will support the implementation of preventive measures and prompt treatment to prevent COVID-19-related morbidity. It may help you get started.

The findings are also highly relevant for analyzing future pandemics and the long-term protective effects of COVID-19 vaccines.

About reviews

In this review, researchers present the results of two large cohort studies evaluating the incidence of autoimmune disease after acute SARS-CoV-2 infection using participants’ electronic medical records.

Pre-study Evidence for Post-COVID Autoimmune Disease

Studies involving pediatric COVID-19 patients suffering from pediatric multisystem inflammatory syndrome (MIS-C) show that COVID-19 results in dysregulated immune responses. The clinical manifestations of MIS-C overlap with hyperinflammatory syndromes such as macrophage activation syndrome, Kawasaki disease, and toxic shock syndrome.

The pathophysiology of COVID-19-associated immune dysfunction includes molecular mimicry by the SARS-CoV-2 protein, due to the presence of the angiotensin-converting enzyme 2 (ACE2) receptor, which is essential for SARS-CoV-2 entry into host cells. Multi-organ involvement, bystander immune cell activation, self-antigen release after tissue injury by SARS-CoV-2, lymphocyte activation by superantigens, and epitope spreading.

Additionally, factors such as genetic susceptibility, age, and comorbidities may contribute to the pathogenesis of COVID-19.

Previous studies comparing immune responses in SARS-CoV-2 infection and autoimmune disease reported that tissue damage in both conditions was largely immunomodulatory, with anti-nuclear antibodies, anti-Ro/SSA Demonstrated by the presence of antibodies, lupus anticoagulants. Cold agglutinin in both conditions.

A retrospective analysis was performed from 31 January 2020 to 30 June 2021 using the Clinical Practice Research Datalink Aurum database. This database contains data from her 458,147 and 1,818,929 SARS-CoV-2 infected and uninfected adults, respectively, living in the UK.

A study preprint reported that the incidence of inflammatory bowel disease, psoriasis, and type 1 diabetes was significantly associated with COVID-19.

Results of Two Cohort Studies Evaluating Post-COVID Autoimmune Disease

Chang et al. utilized her TriNetX health research network of 6 million adults from 48 medical institutions worldwide. The propensity score-matched SARS-CoV-2 infected and uninfected groups each consisted of 887,455 her COVID-19 vaccinees. The incidence of post-COVID-19 autoimmune disease was assessed between 1 January 2020 and 31 December 2021.

At 6-month follow-up, the incidence of autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, vasculitis, type 1 diabetes, and inflammatory bowel disease, was higher than that of SARS-CoV-2 when adjusted for hazard ratio (aHR). 2.99, 2.98, 1.96, 2.68, and 1.78, respectively, which were significantly higher in the infected. The risk of post-COVID autoimmune disease was consistent across ages.

Tesh et al. A yet to be peer-reviewed study to assess the risk of autoimmune disease among 640,701 unvaccinated individuals with polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infection in 2020 Did.

Findings show that COVID-19 patients are 43.0% more likely to develop an autoimmune disease within 3-15.0 months of infection compared to over 1 million age- and gender-matched uninfected individuals shown to be high.

Among autoimmune diseases, vasculitis had the highest incidence rate ratio (IRR) values. Additionally, COVID-19 increased the risk of another autoimmune disease by 23.0% in those with a history of autoimmune disease.

In general, most autoimmune diseases were not specific for COVID-19. However, an important aspect of SARS-CoV-2 infection was the significant rise in the incidence and spectrum of autoimmune diseases following acute COVID-19.

Conclusion

Based on the review’s findings, COVID-19 increases the risk of autoimmune diseases. Due to the retrospective study design, the two cohort studies were unable to provide a causal relationship between his COVID-19 and the development of autoimmune disease.

However, the temporal relationship with COVID-19 history provides reliable and compelling evidence that COVID-19 is associated with increased risk of developing autoimmune diseases.

Health governments and authorities should conduct future research on this topic to obtain national data and increase the generalizability of findings. The critical mechanisms, including genetic and epigenetic predispositions, underlying the association and associated pathophysiology are not fully understood.

However, further studies should be performed using specific gene-deficient animals, bioinformatic analysis, and biological approaches. For example, transcriptome pandemic data should be analyzed to obtain genomic signatures and assess host responses to viral triggers.