Studies on the role of NS3 and NS5A non-structural genes of hepatitis C virus genotype 3a local isolates in apoptosis

Sabri, Sabeen; Idrees, Muhammad; Rafique, Shazia; Ali, Amjad; Iqbal, Mudassar

doi:10.1016/j.ijid.2014.01.010

Cited by 8 publications

(4 citation statements)

References 37 publications

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“…Moreover, HCV proteins (NS5A, NS3, core protein) can interact with p53 (6,18,31,39). Lan et al (18) showed that NS5A protein suppress p53-mediated transcriptional transactivation and apoptosis during HCV infection, which may contribute to hepatocarcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Lan et al (18) showed that NS5A protein suppress p53-mediated transcriptional transactivation and apoptosis during HCV infection, which may contribute to hepatocarcinogenesis. Sabri et al (39) analyzed the interaction of NS3 and NS5A proteins with p53, and they concluded that these HCV proteins play important roles in hepatocarcinogenesis by downregulating expression of the p53 gene. Deng et al (6) found that NS3 protein plays an important role in hepatocarcinogenesis and inhibits p53 function in an NS3 sequence-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

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HCV Infection and Interferon-Based Treatment Induce p53 Gene Transcription in Chronic Hepatitis C Patients

Świątek-Kościelna

Kałużna

Januszkiewicz‐Lewandowska

et al. 2015

Viral Immunology

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It is suggested that the tumor suppressor p53 gene, classified as an interferon-stimulated gene, is implicated in the interferon (IFN)-mediated innate immunity against viruses. This study aimed to examine the transcriptional response of the p53 gene to hepatitis C virus (HCV) infection and IFN-based therapy in chronic hepatitis C (CHC) patients. The study included 65 CHC patients (HCV genotype 1), treated with pegylated IFN-α and ribavirin, and 51 healthy individuals. p53 gene expression was quantified by real-time polymerase chain reaction in peripheral blood mononuclear cells (PBMCs). Analyses were performed before and at weeks 4 and 12 of treatment. p53 gene expression was significantly upregulated in CHC patients compared with healthy controls and at week 4 of therapy. No significant differences in p53 mRNA expression between rapid virologic responders, complete early virologic responders, and nonresponders were observed. No significant correlation was found between p53 gene expression and viral load. The results obtained indicate that HCV infection and IFN-based treatment induces p53 gene transcription in PBMCs. The p53 gene may therefore play a role in HCV infection but is not directly involved in treatment-induced HCV elimination. Moreover, variations in p53 gene expression do not determine on-treatment response in patients with chronic HCV genotype 1 infection.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HCV Infection and Interferon-Based Treatment Induce p53 Gene Transcription in Chronic Hepatitis C Patients

Świątek-Kościelna

Kałużna

Januszkiewicz‐Lewandowska

et al. 2015

Viral Immunology

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“…Considering the combination between NS3 and p53 upregulates UBD expression and UBD is involved with tumorigenesis and malignancy [ 25 , 26 , 31 , 42 ], we wonder whether interfering UBD with RNAi can reverse NS3-mediated development of HCC. To confirm this, we disrupted the expression of UBD with UBD-specific siRNAs in HepG2 cells (shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, overexpressed UBD facilitated HCC proliferation through degrading Wnt-induced secreted protein-1 [ 52 ]. At the same way, NS3, a serine protease, which is responsible for the cleavage of at least four sites (NS3/4A, NS4A/4B, NS4B/5A, and NS5A/5B junctions), has been reported to contribute the development of HCC through inhibiting p53-mediated apoptosis [ 42 ]. In this study, UBD was significantly upregulated by NS3 in HepG2 cells.…”

Section: Discussionmentioning

confidence: 99%

Identification and Verification of Ubiquitin D as a Gene Associated with Hepatitis C Virus-Induced Hepatocellular Carcinoma

Liu

Lin

et al. 2022

Intervirology

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Introduction: Accumulated studies have suggested that hepatitis C virus (HCV) infection is one of the leading causes for hepatocellular carcinoma (HCC). However, the mechanisms underlying the effect of HCV on the occurrence of HCC is still poorly understood. Methods: HCV infection datasets (GSE82177 and GSE17856) and HCC datasets (TCGA-LIHC (The Cancer Genome Atlas Liver Hepatocellular Carcinoma) and GSE89377) were downloaded from Gene Expression Omnibus (GEO) or TCGA for analysis. The common differentially expressed genes (DEGs) in the above four datasets were identified by R software. The expression of Ubiquitin D (UBD) in HCV infected HepG2 cells was detected by RT-qPCR and western blot, respectively. The interaction between NS3 and p53 was detected by Co-Immunoprecipitation. The influence of UBD on the proliferation and migration ability of HepG2 cells was evaluated by CCK-8 and wound healing assay, respectively. Results: UBD was upregulated in both HCV infected samples and HCC samples. HCV NS3 interacted with p53 and inhibited its expression. HCV NS3 induced UBD promoted the proliferation and migration of HepG2 cells. Conclusion: Our results suggest that HCV NS3 induced UBD is positively correlated with the development of HCV-related HCC during HCV infection. Targeting UBD could be a potential strategy for preventing and treating HCV-induced HCC.

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HCV NS3Ag: a reliable and clinically useful predictor of antiviral outcomes in genotype 1b hepatitis C virus-infected patients

Ren

Huang²,

et al. 2016

Eur J Clin Microbiol Infect Dis

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Since hepatitis C virus (HCV) non-structural 3 (NS3) protease inhibitor (PI) combined with pegylated interferon/ribavirin (PR) has been approved for chronic HCV genotype (GT) 1b infection, a reliable and clinically useful predictor combining with serum HCV RNA to predict early virologic response, breakthrough, and relapse is important during HCV antiviral treatment. We evaluated the role of HCV NS3 antigen (HCV NS3Ag) on the prediction of virologic response in patients with HCV GT1b during PR or PR/simeprevir (triple) therapy. Three hundred patients were recruited, and HCV RNA and HCV NS3Ag were tested at baseline and weeks 2, 4, 12, 24, 48, and 72. NS3Ag and HCV RNA were significantly related (r(2) = 0.67) in the whole patient selection. The kinetic pattern of HCV RNA and HCV NS3Ag during triple treatment was similar. HCV NS3Ag levels in the triple group closely followed those of HCV RNA; the r(2) values were 0.756 (baseline), 0.837 (2 weeks), 0.989 (4 weeks), and 0.993 (12 weeks), respectively. For patients treated with PR, the positive and negative predictive values (PPVs and NPVs) for viral response were 96.31 % and 67.19 %, respectively, at week 4 by using the decrease of NS3Ag (dHCV NS3Ag) combined with HCV RNA. At week 12, the PPV was similar at 94.16 %, while the NPV reached 87.26 %. The PPV and NPV for the prediction of relapse and breakthrough were 90.6 % and 76.7 %, respectively. HCV NS3Ag is a valuable marker and could be a supplementary predictor of HCV RNA for the prediction of antiviral response, breakthrough, or relapse during HCV antiviral treatment.

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Studies on the role of NS3 and NS5A non-structural genes of hepatitis C virus genotype 3a local isolates in apoptosis

Abstract: It is concluded that both of the non-structural genes, NS3 and NS5A, of HCV play important roles in the hepatocarcinogenesis of HCV by interacting directly or indirectly in different manners with the p53 gene.

Cited by 8 publications

References 37 publications

HCV Infection and Interferon-Based Treatment Induce p53 Gene Transcription in Chronic Hepatitis C Patients

HCV Infection and Interferon-Based Treatment Induce p53 Gene Transcription in Chronic Hepatitis C Patients

Identification and Verification of Ubiquitin D as a Gene Associated with Hepatitis C Virus-Induced Hepatocellular Carcinoma

HCV NS3Ag: a reliable and clinically useful predictor of antiviral outcomes in genotype 1b hepatitis C virus-infected patients

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