Abstract
The current SARS-CoV-2 pandemic has emerged as an international challenge with strong medical and socioeconomic impact. The spectrum of clinical manifestations of SARS-CoV-2 is wide, covering asymptomatic or mild cases up to severe and life-threatening complications. Critical courses of SARS-CoV-2 infection are thought to be driven by the so-called “cytokine storm”, derived from an excessive immune response that induces the release of proinflammatory cytokines and chemokines. In recent years, non-coding RNAs (ncRNAs) emerged as potential diagnostic and therapeutic biomarkers in both inflammatory and infectious diseases. Therefore, the identification of SARS-CoV-2 miRNAs and host miRNAs is an important research topic, investigating the host–virus crosstalk in COVID-19 infection, trying to answer the pressing question of whether miRNA-based therapeutics can be employed to tackle SARS-CoV-2 complications. In this review, we aimed to directly address ncRNA role in SARS-CoV-2-immune system crosstalk upon COVID-19 infection, particularly focusing on inflammatory pathways and cytokine storm syndromes.
Highlights
SARS-CoV-2 worldwide outbreak in 2019 has become a global challenge
RNA-seq dataset from SARS-CoV-2-infected human cells. They suggested that the expression of eight mature miRNA-like sequences may modulate the host transcriptome upon infection; they indicated as possible targets of SARS-CoV-2 predicted miRNAs, among others, genes linked to the SARS-CoV-2 infection, including angiotensinconverting enzyme 2 (ACE2), CXCL3, JAK2 and STAT2
The authors suggest that upregulated levels of miR-19a/b observed in plasma of SARS-CoV-2-infected patients versus healthy individuals could be involved in the inflammatory storm seen in COVID-19 via inhibition of the immunosuppressive and anti-inflammatory role ensured by transforming growth factor (TGF)-β signaling pathway
Summary
SARS-CoV-2 worldwide outbreak in 2019 has become a global challenge. Old-age males, Hispanic and African American people, as well as patients with history of cardiovascular disease, hypertension, diabetes, obesity, malignancy and chronic diseases (such as kidney disease, arthritis and respiratory diseases) represent a vulnerable cohort of COVID-19 individuals [1]. As reported in studies performed before the pandemic, miR-146a and miR-155 are the first miRNAs enhanced by immune activation in immune cells; they modulate the Toll-Like Receptor (TLR)-signaling pathway, which triggers the production of a large variety of inflammatory cytokines, type I interferons (IFNs) and antiviral proteins through NFkB pathway [39] On this basis, more recently, Roganovic [40] proposed that the downregulation of circulating miR-146a observed in diabetes, obesity and hypertension may explain the more severe COVID-19 cases occurring in these patients. In a study of Jafarinejad-Farsangi et al [43], a few miRNAs, such as miR21, miR-16, let-7b, let-7e and miR-146a were predicted as targeting differentially expressed genes (DEGs) both in lung tissue and post-mortem specimens of patients infected with SARS-CoV-2 Among these genes were STAT1, CCND1, CXCL10 and MAPKAPK2, all engaged in cytokine-involved signaling pathway.
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