The following is a summary of “Interferon gene expression declines over time post-COVID infection and in long COVID patients,” published in the August 2024 issue of Infectious Disease by Gómez-Carballa et al.
Interferons (IFNs) are crucial components of the host’s immune defense against viruses. Its impairment and uncontrolled release of cytokines lead to tissue damage, leading to the progression of coronavirus disease 2019 (COVID-19).
Researchers conducted a retrospective study to examine the role of IFNs and related gene expression patterns in the progression of COVID-19 and patients suffering from long-COVID (LC).
They analyzed IFN gene expression patterns using various IFN gene signatures in 5 patients with acute COVID-19 (n=541) and patients with LC (n=188). The patterns observed in 3 autoimmune diseases, systemic lupus erythematosus (n=242), systemic sclerosis (n=91), and Sjögren’s syndrome (n=282) were compared.
The results showed a strong upregulation of IFN in patients with COVID-19 and autoimmune diseases, which showed time decay in patients with LC. Differential pathway analysis of IFN-related terms exhibited an overactivation of IFN-I/II pathways in autoimmune diseases and IFN-I/II/III pathways in severe COVID-19. On the contrary, these pathways were inactivated or downregulated in LC (IFN-I/III).
They concluded that cytokine exhaustion mediated by the inactivation of IFN gene expression could drive LC.
Source: tandfonline.com/doi/full/10.1080/23744235.2024.2389481
