Peroxisome proliferator-activated receptor γ coactivator family members competitively regulate hepatitis b virus biosynthesis

Shalaby, Rasha E.; Iram, Saira; Oropeza, Claudia E.; McLachlan, Alan

doi:10.1016/j.virol.2018.10.027

Cited by 6 publications

(2 citation statements)

References 60 publications

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“…Among these selected genes, we noticed that SOCS2 , which has been reported to be involved in the replication of RNA viruses, including HCV, 20‐22 and peroxisome proliferator‐activated receptor gamma, coactivator 1 alpha ( PPARGC1A ), which has been shown to be a potent activator of hepatitis B virus biosynthesis, 23 were included on the list of upregulated genes, but not on the list of downregulated genes. At this stage, since we considered that the host factor(s) might participate in the viral replication, we focused on the upregulated genes for further analysis.…”

Section: Resultsmentioning

confidence: 99%

Antiviral mechanism of preclinical antimalarial compounds possessing multiple antiviral activities

et al. 2021

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We previously found that N‐89 and its derivative, N‐251, which are being developed as antimalarial compounds, showed multiple antiviral activities including hepatitis C virus (HCV). In this study, we focused on the most characterized anti‐HCV activity of N‐89(N‐251) to clarify their antiviral mechanisms. We first prepared cells exhibiting resistance to N‐89(N‐251) than the parental cells by serial treatment of HCV–RNA‐replicating parental cells with N‐89(N‐251). Then, we newly generated HCV–RNA‐replicating cells with the replacement of HCV–RNAs derived from N‐89(N‐251)‐resistant cells and parental cells. Using these cells, we examined the degree of inhibition of HCV–RNA replication by N‐89(N‐251) and found that the host and viral factors contributed almost equally to the resistance to N‐89(N‐251). To further examine the contribution of the host factors, we selected several candidate genes by cDNA microarray analysis and found that the upregulated expression of at least RAC2 and CKMT1B genes independently and differently contributed to the acquisition of an N‐89(N‐251)‐resistant phenotype. For the viral factors, we selected several mutation candidates by the genetic comparative analysis of HCV–RNAs and showed that at least one M414I mutation in the HCV NS5B contributed to the resistance to N‐89. Moreover, we demonstrated that the combination of host factors (RAC2 and/or CKMT1B) and a viral factor (M414I mutation) additively increased the resistance to N‐89. In summary, we identified the host and viral factors contributing to the acquisition of N‐89(N‐251)‐resistance in HCV–RNA replication. These findings will be useful for clarification of the antiviral mechanism of N‐89(N‐251).

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Section: Resultsmentioning

confidence: 99%

Antiviral mechanism of preclinical antimalarial compounds possessing multiple antiviral activities

et al. 2021

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“…PGC-1α was shown to mediate the adaptation of HCC cells to hypoxia by promoting mitochondrial biogenesis [104] and mitochondrial biogenesis activated by Sirtuin-1(SIRT1)/PGC-1α was found to foster EMT and HCC metastasis [105]. Activation of PGC-1α is well-known to promote HBV replication [106][107][108][109][110][111], thus possibly promoting HCC development.…”

Section: Peroxisome Proliferator Activated Receptor Co-activators (Pgc-1s)mentioning

confidence: 99%

Mito-Nuclear Communication in Hepatocellular Carcinoma Metabolic Rewiring

Mello

Simeone

Galli

2019

Cells

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As the main metabolic and detoxification organ, the liver constantly adapts its activity to fulfill the energy requirements of the whole body. Despite the remarkable adaptive capacity of the liver, prolonged exposure to noxious stimuli such as alcohol, viruses and metabolic disorders results in the development of chronic liver disease that can progress to hepatocellular carcinoma (HCC), which is currently the second leading cause of cancer-related death worldwide. Metabolic rewiring is a common feature of cancers, including HCC. Altered mito-nuclear communication is emerging as a driving force in the metabolic reprogramming of cancer cells, affecting all aspects of cancer biology from neoplastic transformation to acquired drug resistance. Here, we explore relevant aspects (and discuss recent findings) of mito-nuclear crosstalk in the metabolic reprogramming of hepatocellular carcinoma.

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Hepatitis B Virus Infection: Overview

Yan

Shi

et al. 2019

Advances in Experimental Medicine and Biology

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Peroxisome proliferator-activated receptor γ coactivator family members competitively regulate hepatitis b virus biosynthesis

Cited by 6 publications

References 60 publications

Antiviral mechanism of preclinical antimalarial compounds possessing multiple antiviral activities

Antiviral mechanism of preclinical antimalarial compounds possessing multiple antiviral activities

Mito-Nuclear Communication in Hepatocellular Carcinoma Metabolic Rewiring

Hepatitis B Virus Infection: Overview

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