The identification of microRNAs associated with immune response pathways modulated by ORF8 during SARS-CoV-2 infection: a preliminary in silico analysis.

Coronaviruses (CoV) belong to the Coronaviridae family and comprise four genera, with SARS-CoV-2 being the causative agent of COVID-19. CoV infections can lead to severe respiratory and gastrointestinal diseases. Inflammation is a hallmark of SARS-CoV-2 infection, and accessory proteins have been implicated in modulating the host's immune response. Among these, ORF8 stands out due to its frequent mutations and potential for host adaptation. ORF8 interacts with host proteins promoting the immune escape through downregulation of major histocompatibility complex (MHC) class I molecules, and influences TGF-β1, IFN-beta, and interleukin-17 pathways. Additionally, ORF8 can promote inflammatory factor expression through the activation of NFkB signaling. Host microRNAs (miRNAs), small non-coding RNAs, play an important role in the antiviral responses. Dysregulation of miRNAs is associated with various diseases, including viral infections. Some viruses manipulate host miRNAs to evade immune responses or promote replication. The interaction between host miRNAs and SARS-CoV-2 is an emerging area of research. This study aims to identify host miRNAs potentially regulating immune response pathways during SARS-CoV-2 infection, including MHC class I, IRF3, IL17, IFNβ, and LTBP1, with in vitro validation in serum from COVID-19 patients. Understanding miRNA-mediated regulation in COVID-19 may offer insights into therapeutic strategies.