Hepatitis B virus prevents excessive viral production via reduction of cell death-inducing DFF45-like effectors

Yasumoto, Jun; Kasai, Hirotake; Yoshimura, Kenichi; Otoguro, Teruhime; Watashi, Koichi; Wakita, Takaji; Yamashita, Atsuya; Tanaka, Tomohisa; Takeda, Sén; Moriishi, Kohji

doi:10.1099/jgv.0.000813

Cited by 12 publications

(15 citation statements)

References 48 publications

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“…Apart from reports that HBV increased lipogenesis, several other studies showed that HBV infection also increased fatty acid oxidation and reduced lipid droplets (LD) formation. Yasumoto et al (2017) showed that the content of intracellular TGs and the average size of a single LD were significantly reduced in HBV-infected or transfected cells compared to control cells, and that was because of decreased levels of proteins involved in LD expansionary and lipid storage. Studies also showed that HBV replication increased adiponectin expression (a downstream gene of PPARγ) (Yoon et al, 2011).…”

Section: Hbv-induced Changes In Fatty Acid Metabolismmentioning

confidence: 99%

Multifaceted Interaction Between Hepatitis B Virus Infection and Lipid Metabolism in Hepatocytes: A Potential Target of Antiviral Therapy for Chronic Hepatitis B

et al. 2021

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Hepatitis B virus (HBV) is considered a “metabolic virus” and affects many hepatic metabolic pathways. However, how HBV affects lipid metabolism in hepatocytes remains uncertain yet. Accumulating clinical studies suggested that compared to non-HBV-infected controls, chronic HBV infection was associated with lower levels of serum total cholesterol and triglycerides and a lower prevalence of hepatic steatosis. In patients with chronic HBV infection, high ALT level, high body mass index, male gender, or old age was found to be positively correlated with hepatic steatosis. Furthermore, mechanisms of how HBV infection affected hepatic lipid metabolism had also been explored in a number of studies based on cell lines and mouse models. These results demonstrated that HBV replication or expression induced extensive and diverse changes in hepatic lipid metabolism, by not only activating expression of some critical lipogenesis and cholesterolgenesis-related proteins but also upregulating fatty acid oxidation and bile acid synthesis. Moreover, increasing studies found some potential targets to inhibit HBV replication or expression by decreasing or enhancing certain lipid metabolism-related proteins or metabolites. Therefore, in this article, we comprehensively reviewed these publications and revealed the connections between clinical observations and experimental findings to better understand the interaction between hepatic lipid metabolism and HBV infection. However, the available data are far from conclusive, and there is still a long way to go before clarifying the complex interaction between HBV infection and hepatic lipid metabolism.

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Section: Hbv-induced Changes In Fatty Acid Metabolismmentioning

confidence: 99%

Multifaceted Interaction Between Hepatitis B Virus Infection and Lipid Metabolism in Hepatocytes: A Potential Target of Antiviral Therapy for Chronic Hepatitis B

et al. 2021

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“…Adiponectin protects against IR; thus, it is inversely associated with BMI, T2DM, and several metabolic disorders, such as cardiovascular disease and atherosclerosis [ 41 ]. Additionally, a study reported that HBV may influence lipid deposition and lipid droplet size in hepatocytes by decreasing the expression of cell death-inducing DFF45-like effectors (CIDEs) B and C (CIDEB and CIDEC), which are involved in lipid droplet expansion for improving lipid storage [ 42 ]. Thus, the increased risk and progression of both fatty liver and coronary disease should be carefully monitored when treating patients with chronic HBV and NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Abnormal transaminase and lipid profiles in coexisting diseases in patients with fatty liver: a population study in Sichuan

Jiang

Liu

et al. 2021

Bioscience Reports

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Among chronic liver diseases, fatty liver has the highest incidence worldwide. Coexistence of fatty liver and other chronic diseases, such as diabetes, hepatitis B virus (HBV) and Helicobacter pylori (Hp) infection, is common in clinical practice. The present study was conducted to analyze the prevalence and association of coexisting diseases in patients with fatty liver and to investigate how coexisting diseases contribute to abnormal transaminase and lipid profiles. We enrolled participants who were diagnosed with fatty liver via ultrasound in the physical examination center of West China Hospital. Multivariable logistic regression was used to determine the adjusted odds ratios (ORs). We found that 23.6% of patients who underwent physical examinations were diagnosed with fatty liver. These patients had higher risks of metabolic syndrome (MetS), type 2 diabetes mellitus (T2DM), and hypertension and a lower risk of HBV infection. The risks of Hp infection and hyperthyroidism did not statistically differ. When fatty liver coexisted with T2DM, MetS and thyroid dysfunction, it conferred a higher risk of elevated transaminase. Fatty liver was positively correlated with triglycerides, cholesterol and low-density lipoprotein cholesterol (LDL-C) and negatively correlated with HBV; thus, HBV had a neutralizing effect on lipid metabolism when coexisting with fatty liver. In conclusion, patients with fatty liver that coexists with T2DM, MetS and thyroid dysfunction are more prone to elevated transaminase levels. Patients with both fatty liver and HBV may experience a neutralizing effect on their lipid metabolism. Thus, lipid alterations should be monitored in these patients during antiviral treatment for HBV.

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“…Yasumoto et al reported that CIDEB and CIDEC positively regulate cellular LD size. Overexpression of CIDEB or CIDEC enhanced HBV production in HBV-infected cells (HepG2.2.15), and deficiency in CIDEB or CIDEC impaired HBV production and reduced the size of single LDs [ 62 ]. Yasumoto et al also suggested that impairment of CIDE expression might stabilize an appropriate production level of HBV and inhibit excessive HBV productions [ 62 ].…”

Section: Hepatitis Viruses and Cholesterol Metabolismmentioning

confidence: 99%

“…Overexpression of CIDEB or CIDEC enhanced HBV production in HBV-infected cells (HepG2.2.15), and deficiency in CIDEB or CIDEC impaired HBV production and reduced the size of single LDs [ 62 ]. Yasumoto et al also suggested that impairment of CIDE expression might stabilize an appropriate production level of HBV and inhibit excessive HBV productions [ 62 ]. Experimental results from HBV-inducible Hep38.7-Tet cells incubated with HBV suggested that HBV production may affect the expression of CIDE proteins in hepatocytes, and CIDE proteins were found to significantly enhance the activity of HBV core promoter [ 62 ].…”

Section: Hepatitis Viruses and Cholesterol Metabolismmentioning

confidence: 99%

Viral Hepatitis, Cholesterol Metabolism, and Cholesterol-Lowering Natural Compounds

Liou

Mani

Yen

2022

IJMS

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Hepatitis is defined as inflammation of the liver; it can be acute or chronic. In chronic cases, the prolonged inflammation gradually damages the liver, resulting in liver fibrosis, cirrhosis, and sometimes liver failure or cancer. Hepatitis is often caused by viral infections. The most common causes of viral hepatitis are the five hepatitis viruses—hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV). While HAV and HEV rarely (or do not) cause chronic hepatitis, a considerable proportion of acute hepatitis cases caused by HBV (sometimes co-infected with HDV) and HCV infections become chronic. Thus, many medical researchers have focused on the treatment of HBV and HCV. It has been documented that host lipid metabolism, particularly cholesterol metabolism, is required for the hepatitis viral infection and life cycle. Thus, manipulating host cholesterol metabolism-related genes and proteins is a strategy used in fighting the viral infections. Efforts have been made to evaluate the efficacy of cholesterol-lowering drugs, particularly 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, in the treatment of hepatitis viral infections; promising results have been obtained. This review provides information on the relationships between hepatitis viruses and host cholesterol metabolism/homeostasis, as well as the discovery/development of cholesterol-lowering natural phytochemicals that could potentially be applied in the treatment of viral hepatitis.

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Hepatitis B virus prevents excessive viral production via reduction of cell death-inducing DFF45-like effectors

Cited by 12 publications

References 48 publications

Multifaceted Interaction Between Hepatitis B Virus Infection and Lipid Metabolism in Hepatocytes: A Potential Target of Antiviral Therapy for Chronic Hepatitis B

Multifaceted Interaction Between Hepatitis B Virus Infection and Lipid Metabolism in Hepatocytes: A Potential Target of Antiviral Therapy for Chronic Hepatitis B

Abnormal transaminase and lipid profiles in coexisting diseases in patients with fatty liver: a population study in Sichuan

Viral Hepatitis, Cholesterol Metabolism, and Cholesterol-Lowering Natural Compounds

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