Background: HBV, a contagious infection, causes chronic hepatitis, cirrhosis, and hepatocellular cancer in many people. The WHO estimates that 2 billion people are exposed to HBV annually, depending on when. The Hepadnaviridae family virus has an unfinished 3.2-kilobase double-stranded DNA molecule. Increased ALT, AST, and HBsAg positive or HBV DNA viral load are used to identify the illness. Despite global immunization campaigns, nations with low vaccination coverage and no diagnosis remain concerned. The worldwide HBV burden remains high. MicroRNAs (miRNAs) bind to mRNAs after transcription to govern gene expression, hepatitis B virus replication, and extracellular matrix development.Methods: Sixty six Iraqi HBV patients were involved in a case-sectional control study. From September 2021 to February 2022, blood samples were taken from Al-Yarmook Teaching Hospital and Central Public Health Laboratory in Baghdad. ELISA verified HBV markers, HBsAg, HBsAb, HBeAg, HBeAb, and HBcAb in all samples, and real-time PCR estimated viral load from DNA. The research found that miR122 and miR150 gene expressions affect HBV fibrosis severity.Results: The gene expression of miR-122 and miR-150 was found using RT-PCR after normalization with Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a common housekeeping gene. The analysis of variance found substantial differences between patients and controls. The research found a considerable downregulation of miRNA-122 and miRNA-150 in HBV-infected individuals.Conclusions: Depending on HBV severity, miRNA levels may vary. HBV patients, especially those with fibrosis and chronic HBV, have reduced miR122 and miR150. MiR-122 and miR-150 may be interesting HBV diagnostic, fibrosis progression, and therapeutic targets.Keywords: Hepatitis B virus; MicroRNAs (miRNAs); RT-PCR; Primers; Gene expression; Liver disease
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