Atousa Ghorbani - Department of biology, Faculty of basic sciences, East Tehran Branch (Ghiamdasht), Islamic Azad University, Tehran, Iran
Shadi Rabiee - Department of biology, Faculty of basic sciences, East Tehran Branch (Ghiamdasht), Islamic Azad University, Tehran, Iran

Backgrounds: In individuals, the receptor heterodimer (IFNR۱-IFNR۲) trigged the immunesystem in response to cytokines or pathogens. Type I IFNs mediate their activity by binding todimeric receptor composed IFNAR۱/۲, activating JAKs kinases and phosphorylating STAT ۱/۲,which in turn, lead to transcription of IFN-signature genes (ISG). The type I interferons wereknown as the first cytokines discovered and named for their powerful ability to inhibit viralreplication. Insufficient virus-induced type I IFN production is characteristic of severe diseasecaused by SARS-CoV-۲. Also, previous studies in COVID۱۹ patients with a dysfunctionalimmune response showed that there is a massive chemokine and cytokine release, referred to asthe ‘cytokine storm’. So based on studies IFNAR۲ can assist to identify severe illness due toSARS-COV-۲ and help to develop an effective drug against the infection.Materials and Methods: To find the bioinformatics relationship between these two components(Gene, miRNA) NCBI sites, miRBase, miRWALK۲.۰, and DAVID were used.Results: Studies done on the hsa-miR-۱۴۶a-۳p determined that this microRNA binds to the ۳UTR of the IFNAR۲ gene transcription with great power and acts on its inhibitory action.Conclusion: Studies done on the hsa-miR-۱۴۶a-۳p determined that this microRNA binds to the۳ UTR of the IFNAR۲ gene transcription with great power and acts on its inhibitory action theexpected expression of IFNAR۲ and the negative regulatory function of the microRNAs wouldbe expected. The expression of hsa-miR-۱۴۶a-۳p is expected to decrease and consequentlyincrease the expression of the target gene and activation in the “JAK-STAT Signalingpathways”.

Bioinformatics, COVID-۱۹, hsa-miR-۱۴۶a-۳p, IFNAR۲ gene, miRNA, SARS-COV- ۲