Toll-like receptor 7 and RIG-I-like receptors expression in peripheral blood mononuclear cells of naïve patients with hepatitis C

• Published in: BMC research notes Vol. 16; no. 1; pp. 1 - 344
• Main Authors: Gilanipour, Atena, Teimoori, Ali, Arabzadeh, Seyed Alimohammad, Mollaie, Hamid Reza, Mousavi, Elham
• Format: Journal Article
• Language: English
• Published: London BioMed Central Ltd 22.11.2023; BioMed Central; BMC
• Subjects: Disease; Gene expression; Genes; Genetic engineering; Hepatitis C; Hepatitis C virus; Immune system; Infections; Innate immunity; Leukocytes (mononuclear); Pathogens; Pattern recognition receptors; Peripheral blood mononuclear cells; Polymerase chain reaction; Receptor mechanisms; RIG-I-like receptors; Thermal cycling; TLR7 protein; Toll-like receptor7; Toll-like receptors; Viral infections; Iran; Germany
• ISSN: 1756-0500; 1756-0500
• DOI: 10.1186/s13104-023-06626-2

The proper function of Pattern Recognition Receptors (PRRs) as a part of the host immune system can eliminate numerous pathogens from the body. However, some viruses can manipulate PRRs to escape the innate immune system. As there is controversy in the activation of PRRs in patients infected with HCV, we decided to evaluate the gene expression changes of PRRs in HCV cases compared to the healthy control. In this study, the relative expression of Toll-like receptor 7, RIG-I, and MAD-5 in peripheral mononuclear blood cells of twenty HCV patients and twenty healthy controls of the same gender and age were analyzed by quantitative Real-time PCR. Our results showed that the expression of RIG-I and MAD-5 significantly increased in HCV-infected samples compared to the controls (P value:0.01; P value:0.05), while the expression of TLR7 was similar between the case and the control group (P value:0.1). It seems in suppressing HCV, RIG-I and MAD-5 receptors are likely to be more activated than TRL7 in HCV patients. The lack of TLR7 gene expression might reflect the defect of the host in the stimulation of the innate immune system through the TLR7 pathway.