Related Experiment Video
Updated: May 1, 2026
A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
Distinct Toll-like Receptor 3 and 7 Expression in Peripheral Blood Mononuclear Cells From Patients with Chronic
Mahsa Motavaf1, Fatemeh Noorbakhsh2, Seyed Moayed Alavian3
1Department of Microbiology, Islamic Azad University of Varamin-Pishva, Varamin, IR Iran ; Department of Molecular Hepatology, Middle East Liver Disease Center (MELD), Tehran, IR Iran.
Insights
Hepatitis C virus (HCV) infection is linked to lower expression of Toll-like receptors (TLRs) 3 and 7 in immune cells. This reduction may help HCV evade the body's innate immune defenses.
Area of Science:
- Immunology
- Virology
- Hepatology
Background:
- Hepatitis C virus (HCV) causes chronic liver disease affecting millions globally.
- Toll-like receptors (TLRs) are crucial for innate immunity, recognizing pathogens like HCV and triggering antiviral responses.
- TLR activation leads to the production of antiviral and pro-inflammatory cytokines.
Purpose of the Study:
- To compare the expression levels of TLR3 and TLR7 in patients with chronic HCV infection versus healthy individuals.
- To investigate the role of TLR3 and TLR7 in the context of HCV-induced immune evasion.
Main Methods:
- Case-control study involving 25 chronic HCV patients and 25 healthy controls.
- Peripheral blood mononuclear cells (PBMCs) were isolated for RNA extraction.
- Quantitative real-time PCR was used to measure relative TLR3 and TLR7 gene expression, normalized to GAPDH.
Main Results:
- TLR3 expression was significantly lower in HCV patients (6.23 ± 0.91) compared to controls (3.89 ± 0.85; P < 0.001).
- TLR7 expression was also significantly lower in HCV patients (1.48 ± 0.82) versus controls (1.33 ± 1.18; P < 0.001).
- Both TLR3 and TLR7 showed significantly reduced expression in individuals with chronic HCV infection.
Conclusions:
- Decreased expression of TLR3 and TLR7 may represent a mechanism by which HCV evades the host's innate immune system.
- These findings highlight a potential role for TLR dysregulation in the pathogenesis of chronic HCV infection.
Background:
Hepatitis C virus (HCV) is a major cause of chronic liver disease, with around 130 million infected people worldwide. HCV is recognized by Toll-like receptors (TLRs), which are key mediators of innate immune response. Up on activation of TLRs, anti-viral cytokines and pre-inflammatory are produced.
Objectives:
In this study, we compared the expression levels of two members of the TLR family (TLR3 and TLR7) that recognize viral RNA in peripheral blood mononuclear cell (PBMC) of patients with chronic HCV infection and healthy controls.
Patients And Methods:
In this case-control study, blood samples were collected from patients admitted to Blood Transfusion Research Center, Tehran, Iran. PBMC was isolated from blood of chronic HCV patients (n = 25) and age and sex-matched healthy controls (n = 25). RNA was extracted from PBMC and cDNA was synthesized from total RNA templates using reverse transcriptase. The relative level of expression was quantified by real-time PCR using Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as reference gene and the results were compared by Pfaffl method. Data were analyzed using non-parametric Wilcoxon test. P < 0.05 was considered significant.
Results:
In both groups, we had 13 males and 12 females with a mean age of 48.7 ± 16. TLR3 (6.23 ± 0.91 vs. 3.89 ± 0.85, P < 0.001) and TLR7 (1.48 ± 0.82 vs-1.33 ± 1.18, P < 0.001) expressions were significantly lower in patients with chronic HCV infection when compared with healthy controls.
Conclusions:
This study suggests that decrease in levels of TLR3 and TLR7 expression is a mechanism that may enable HCV to evade the host innate immune response.
