Characterization of the expression of the hepatitis C virus F protein

Roussel, J; Pillez, André; Montpellier, Claire; Duverlie, Gilles; Cahour, Annie; Dubuisson, Jean; Wychowski, Czeslaw

doi:10.1099/vir.0.19065-0

Cited by 52 publications

(66 citation statements)

References 45 publications

(40 reference statements)

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“…T7 RNA polymerase has shown varying levels of frameshifting [e.g. 12-15 % +1 frameshifting and 30-45 % 21 frameshifting in a study by Choi et al (2003) and 30 % +1 frameshifting described by Roussel et al (2003)]. By measuring luciferase activity, we found 11 % +1 frameshifting and 20 % 21 frameshifting with the same polymerase.…”

Section: Discussionmentioning

confidence: 71%

Transcriptional slippage prompts recoding in alternate reading frames in the hepatitis C virus (HCV) core sequence from strain HCV-1

Ratinier

Boulant²,

Combet

et al. 2008

Journal of General Virology

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Since the first report of frameshifting in HCV-1, its sequence has been the paradigm for examining the mechanism that directs alternative translation of the hepatitis C virus (HCV) genome. The region encoding the core protein from this strain contains a cluster of 10 adenines at codons 8-11, which is thought to direct programmed ribosomal frameshifting (PRF), but formal evidence for this process has not been established unequivocally. To identify the mechanisms of frameshifting, this study used a bicistronic dual luciferase reporter system in a coupled transcription/translation in vitro assay. This approach revealed +1 as well as -1 frameshifting, whereas point mutations, selectively introduced between codons 8 and 11, demonstrated that PRF did not readily account for frameshifting in strain HCV-1. Sequence analysis of cDNAs derived from RNA transcribed by T7 RNA polymerase in the dual luciferase reporter system, as well as in both a subgenomic replicon and an infectious clone derived from strain JFH1, identified additions and deletions of adenines between codons 8 and 11 due to transcriptional slippage (TS). Moreover, RNA isolated from cells infected with virus generated by JFH1 containing the A-rich tract also contained heterogeneity in the adenine sequence, strongly suggesting TS by the NS5B viral polymerase. These findings have important implications for insight into frameshifting events in HCV-1 and demonstrate for the first time the involvement of transcriptional slippage in this recoding event.

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Section: Discussionmentioning

confidence: 71%

Transcriptional slippage prompts recoding in alternate reading frames in the hepatitis C virus (HCV) core sequence from strain HCV-1

Ratinier

Boulant²,

Combet

et al. 2008

Journal of General Virology

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“…F protein is a short-lived endoplasmic reticulum-associated protein, and its stability can be maintained by the use of the proteasome inhibitor MG132 (22). The functional significance of F protein remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C virus F protein: A double-edged sword in the potential contribution of chronic inflammation to carcinogenesis

Kong

Deng²,

Wang³

et al. 2009

Mol Med Rep

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“…Localization studies have revealed that core+1/ARFP isoforms can be found in the cytoplasm, associated either with the endoplasmic reticulum membrane (Roussel et al, 2003;Xu et al, 2003;Vassilaki et al, 2007Vassilaki et al, , 2008aMa et al, 2008) or with mitochondria (Ratinier et al, 2009), but not inside the nucleus. Therefore and similarly to core, core+1/ARFP must exert its transcriptional effect indirectly.…”

Section: Ryanmentioning

confidence: 99%

Hepatitis C virus core+1/ARF protein decreases hepcidin transcription through an AP1 binding site

Kotta‐Loizou

Vassilaki

Pissas

et al. 2013

Journal of General Virology

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Chronic viral hepatitis C is characterized by iron accumulation in the liver, and hepcidin regulates iron absorption. Hepatitis C virus (HCV) core+1/ARFP is a novel protein produced by a second functional ORF within the core gene. Here, using reporter assays and HCV bicistronic replicons, we show that, similarly to core, core+1/ARFP decreases hepcidin expression in hepatoma cells. The activator protein 1 (AP1) binding site of the human hepcidin promoter, shown here to be relevant to basal promoter activity and to the repression by core, is essential for the downregulation by core+1/ARFP while the previously described C/EBP (CCAAT/enhancer binding protein) and STAT (signal transducer and activator of transcription) sites are not. Consistently, expression of the AP1 components c-jun and c-fos obliterated the repressive effect of core and core+1/ARFP. In conclusion, we provide evidence that core+1/ARFP downregulates AP1-mediated transcription, providing new insights into the biological role of core+1/ARFP, as well as the transcriptional modulation of hepcidin, the main regulator of iron metabolism.

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Characterization of the expression of the hepatitis C virus F protein

Cited by 52 publications

References 45 publications

Transcriptional slippage prompts recoding in alternate reading frames in the hepatitis C virus (HCV) core sequence from strain HCV-1

Transcriptional slippage prompts recoding in alternate reading frames in the hepatitis C virus (HCV) core sequence from strain HCV-1

Hepatitis C virus F protein: A double-edged sword in the potential contribution of chronic inflammation to carcinogenesis

Hepatitis C virus core+1/ARF protein decreases hepcidin transcription through an AP1 binding site

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