Hepatitis B Virus Protein X-induced Expression of the CXC Chemokine IP-10 Is Mediated through Activation of NF-κB and Increases Migration of Leukocytes

Zhou, Yu; Wang, Shuo; Ma, Jingwei; Zhang, Lei; Zhu, Hong-Jian; Lei, Ping; Yang, Zhonghan; Zhang, Biao; XinXin, Yao; Shi, Chuan; Sun, Lifang; Wu, Xue-Ru; Ning, Qin; Shen, Guanxin; Huang, Bo

doi:10.1074/jbc.m109.067629

Cited by 56 publications

(42 citation statements)

References 50 publications

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“…Furthermore, inhibition of HBV replication by TNF-α treatment could involve NF-κB activation (Biermer et al 2003;Slagle et al 2014). NF-κB activation by HBx alone (in the absence of HBV replication) could result in cytokine productions of IL-6, IP-10, and IL23 (Lee and Koretzky 1998;Zhou et al 2010b;Xia et al 2012). We speculate here that the inhibitory effect of NF-κB on HBV could be mediated in part via miR-130a.…”

Section: Discussionmentioning

confidence: 96%

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ

Huang

Chou

Lee

et al. 2015

RNA

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In hepatitis B virus (HBV)-replicating hepatocytes, miR-130a expression was significantly reduced. In a reciprocal manner, miR130a reduced HBV replication by targeting at two major metabolic regulators PGC1α and PPARγ, both of which can potently stimulate HBV replication. We proposed a positive feed-forward loop between HBV, miR-130a, PPARγ, and PGC1α. Accordingly, HBV can significantly enhance viral replication by reducing miR-130a and increasing PGC1α and PPARγ. NF-κB/ p65 can strongly stimulate miR-130a promoter, while miR-130a can promote NF-κB/p65 protein level by reducing PPARγ and thus NF-κB/p65 protein degradation. We postulated another positive feed-forward loop between miR-130a and NF-κB/p65 via PPARγ. During liver inflammation, NF-κB signaling could contribute to viral clearance via its positive effect on miR-130a transcription. Conversely, in asymptomatic HBV carriers, persistent viral infection could reduce miR-130a and NF-κB expression, leading to dampened inflammation and immune tolerance. Finally, miR-130a could contribute to metabolic homeostasis by dual targeting PGC1α and PPARγ simultaneously.

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Section: Discussionmentioning

confidence: 96%

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ

Huang

Chou

Lee

et al. 2015

RNA

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“…Other viruses have been shown to activate TAK1 to induce downstream signaling pathways. For example, hepatitis B virus protein X (HBx) induces the activation of NF-B through a TRAF2/TAK1 signaling pathway (85). Although the human T lymphotropic virus (HTLV) oncoprotein Tax constitutively activates TAK1, the role of TAK1 in NF-B activation induced by Tax is not clear.…”

Section: Discussionmentioning

confidence: 99%

Phosphorylation and Polyubiquitination of Transforming Growth Factor β-Activated Kinase 1 Are Necessary for Activation of NF-κB by the Kaposi's Sarcoma-Associated Herpesvirus G Protein-Coupled Receptor

Bottero

Kerur

Sadagopan

et al. 2011

J Virol

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“…Regarding the involvement of viral components with the expression pattern of RANTES and IP-10, our data are in contrast to those of Wang et al (2010) but at par with those of Zhang et al (2009), since we did not observe any association of mRNA expression pattern of either of the chemokines with the level of serum HBsAg or HBV DNA in our study subjects. This finding seems not to be unlikely on the basis of reported involvement of HBV X protein (HBX) regulating the expression of IP-10 through activation of NF-κB pathway (Zhou, 2010).…”

mentioning

confidence: 88%

“…In contrast, induced expression of both RANTES and IP-10 genes have been shown to be associated with HBV clearance . It has also been documented that HBV protein X (HBx) increases IP-10 expression in a dose-dependent manner through the modulation of NF-ķB pathway (Zhou, 2010). Despite the addition of new insight into the viral and host factors that determine pathogenesis and outcome of HBV infection, information regarding the level of expression of RANTES and IP-10 mRNA in various stages of HBV infection is still scanty.…”

Section: Introductionmentioning

confidence: 99%

Reduced Expression of Human Chemokine Genes RANTES and IP-10 in Hepatitis B Virus Mediated Cirrhosis of Liver

Shravanti¹,

Mukherjee²,

Rao³

et al. 2012

JBLS

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Regulated upon Activation Normal T cell Expressed and Secreted (RANTES) and interferon gamma inducible protein 10 (IP-10), both chemokines are chemotactic for immunocompetent cells and play an important role in cell mediated antiviral defense. The objective of this work was to assess the expression pattern of RANTES and IP-10 genes in peripheral blood mononuclear cells (PBMCs) of hepatitis B virus (HBV) infected patients having various ISSN 2157-6076 2012 www.macrothink.org/jbls 221 disease severity. The study was performed on 79 HBV infected patients grouped into acute, inactive carriers (IC), chronic (CHB), cirrhosis and hepatocellular carcinoma (HCC) plus 41 healthy voluntary blood donors as controls. Quantification of HBV surface antigen (HBsAg) was done by a sandwich enzyme linked immunosorbent assay (ELISA). Conventional and real time polymerase chain reaction (PCR) were used for genotyping and determination of HBV DNA load respectively. RANTES and IP-10 mRNA expressions were evaluated by reverse transcription PCR (RT-PCR) and densitometry. Results obtained show that RANTES expression reduced significantly (p<0.0001) in cirrhosis group in comparison to controls and remain unaltered in other disease categories. Reduction in IP-10 expression was significant (p=0.006) in patients of all disease categories than controls which was most evident in cirrhosis group (p<0.0001). No association was found between the expression level of chemokines with HBV genotypes, HBsAg and HBV DNA levels in sera. Journal of Biology and Life ScienceIt could be concluded that reduced expression of both the chemokines might be associated with lesser infiltration of immunocompetent cells to liver to avert further damage in cirrhosis.Serum level of both RANTES and IP-10 can be considered as prognostic marker of liver cirrhosis by validation studies.

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Hepatitis B Virus Protein X-induced Expression of the CXC Chemokine IP-10 Is Mediated through Activation of NF-κB and Increases Migration of Leukocytes

Cited by 56 publications

References 50 publications

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ

Phosphorylation and Polyubiquitination of Transforming Growth Factor β-Activated Kinase 1 Are Necessary for Activation of NF-κB by the Kaposi's Sarcoma-Associated Herpesvirus G Protein-Coupled Receptor

Reduced Expression of Human Chemokine Genes RANTES and IP-10 in Hepatitis B Virus Mediated Cirrhosis of Liver

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