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2016 ; 11
(5
): e0154512
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Transcriptional Dysregulation of Upstream Signaling of IFN Pathway in Chronic HCV
Type 4 Induced Liver Fibrosis
#MMPMID27135246
Ibrahim MK
; Salum GM
; Bader El Din NG
; Dawood RM
; Barakat A
; Khairy A
; El Awady MK
PLoS One
2016[]; 11
(5
): e0154512
PMID27135246
show ga
IFN orchestrates the expression of various genes to halt hepatitis C virus (HCV)
replication with the possibility of either reduced or increased liver fibrosis;
due to controlled viral replication or overproduction of inflammatory mediators,
repectively. In this study, we examined the transcriptional profiling of type I
IFN related genes in HCV-chronically infected patients with varying degrees of
liver fibrosis. PCR array was used to examine the expression of 84 type I IFN
related genes in peripheral blood mononuclear cells (PBMCs) RNA from 12
treatment-naïve chronic HCV patients (5 F0-F1 and 7 F2-F4) and 5 healthy
subjects. We further validated our results by quantitative real time PCR
(qRT-PCR) in 103 treatment-naïve chronic HCV patients (43 F0-F1 and 60 F2-F4) and
15 controls. PCR array data revealed dysregulation in TLR7 pathway. The
expression of TLR7 was decreased by 4 folds and MyD88 was increased by 3 folds in
PBMCs of F2-F4 patients when compared to the healthy volunteers (p = 0.03 and
0.002, respectively). In addition, IRF7 and TLR7 showed dramatic downregulation
(6 and 8 folds, respectively) in F2-F4 patients when compared to F0-F1 ones.
qRT-PCR confirmed the altered expression patterns of TLR7 and MyD88 in F2-F4
patients when compared to either controls or F0-F1 patients. However, by qRT-PCR,
IRF7 and NF-?B1 (TLR7 pathway transcription factors) exhibited similar mRNA
abundance among F2-F4 and F0-F1 patients. These results suggest that TLR7 and
MyD88 are possible candidates as biomarkers for the progression of HCV-induced
liver fibrosis and/ or targets for therapeutic intervention.
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