Reduced expression of TRIF in chronic HBV infected Iranian patients

Abstract

Background and aims: TRIF is one of the main intracellular adaptor proteins required for TLR3 and 4 signaling. Abnormal gene expression of TRIF may lead to abrogated immune responses against viral infections including hepatitis B infection. The aim of this study was to identify the mRNA levels of TRIF in PBMCs isolated from chronic HBV (CHB) infected patients.

Material and methods: mRNA was isolated from 63 CHB patients and 60 healthy controls and transcript levels of TRIF were examined in parallel with beta-actin (as housekeeping gene) using Real-Time PCR techniques.

Results: Our results demonstrated that expression of TRIF was significantly decreased in PBMCs isolated from CHB patients when compared to healthy controls.

Conclusions: Based on the results reported here, it seems that CHB patients are unable to express appropriate levels of the TRIF gene, which may attenuate TLR3 and 4 signaling subsequent to HBV infection. Our results suggest a possible mechanism, which may explain why hepatitis B infection is stable in CHB patients.

Keywords: HBV; Hepatitis B virus; IRAK1; IRF3; Interferon regulatory transcription factor 3; Interleukin-1 receptor associated kinase-1; MYD88; NF-κB; Nuclear factor kappa-light-chain-enhancer of activated B cells; PAMP; PBMC; TIR-domain-containing adapter-inducing interferon-β; TLR; TNF receptor associated factor; TRAF6; TRIF; Toll Like Receptor; myeloid differentiation primary response; pathogen associated molecular patterns; peripheral blood mononuclear cell.