Therapeutic role of miR-19a/b protection from influenza virus infection in patients with coronary heart disease.

Publication date: Mar 12, 2024

Patients with pre-existing medical conditions are at a heightened risk of contracting severe acute respiratory syndrome (SARS), SARS-CoV-2, and influenza viruses, which can result in more severe disease progression and increased mortality rates. Nevertheless, the molecular mechanism behind this phenomenon remained largely unidentified. Here, we found that microRNA-19a/b (miR-19a/b), which is a constituent of the miR-17-92 cluster, exhibits reduced expression levels in patients with coronary heart disease in comparison to healthy individuals. The downregulation of miR-19a/b has been observed to facilitate the replication of influenza A virus (IAV). miR-19a/b can effectively inhibit IAV replication by targeting and reducing the expression of SOCS1, as observed in cell-based and coronary heart disease mouse models. This mechanism leads to the alleviation of the inhibitory effect of SOCS1 on the interferon (IFN)/JAK/STAT signaling pathway. The results indicate that the IAV employs a unique approach to inhibit the host’s type I IFN-mediated antiviral immune responses by decreasing miR-19a/b. These findings provide additional insights into the underlying mechanisms of susceptibility to flu in patients with coronary heart disease. miR-19a/b can be considered as a preventative/therapy strategy for patients with coronary heart disease against influenza virus infection.

Concepts Keywords
Coronary coronary heart disease
Downregulation influenza virus
Healthy innate immunity
Influenza miR-19a/19b
Molecular MT: non-coding RNAs
SOCS1

Semantics

Type Source Name
disease MESH influenza
disease MESH virus infection
disease MESH coronary heart disease
disease MESH severe acute respiratory syndrome
disease VO Viruses
disease MESH disease progression
disease IDO replication
drug DRUGBANK Influenza A virus
disease IDO cell
disease IDO host
disease IDO susceptibility

Original Article

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