Dexamethasone Stimulates Hepatitis B Virus (HBV) Replication Through Autophagy

He, Qiao; Song, Xiaoyu; Huang, Yecai; Huang, Wenjuan; Ye, Bo; Luo, Huaichao; Luo, Hao; Wu, Lei; Wang, Zuo; Chen, Weixian; Zhang, Li

doi:10.12659/msm.906250

Cited by 21 publications

(17 citation statements)

References 32 publications

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“…In chronic infection, HBV can activate autophagy through different pathways, 100 promoting the replication of HBV and the formation and release of virus particles, thus aggravating the disease process. [101][102][103] For example, HBs can activate autophagy by triggering endoplasmic reticulum stress. 104 HBx can enhance autophagy and promote viral replication by binding to PI3KC3 or by activating miR-192-3p-XIAP signaling.…”

Section: Hbv and Autophagymentioning

confidence: 99%

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

Yu¹,

Han²,

Zhao³

et al. 2021

JHC

115

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Hepatocellular carcinoma (HCC) is a common malignancy, and the hepatitis B virus (HBV) is its major pathogenic factor. Over the past decades, it has been confirmed that HBV infection could promote disease progression through a variety of mechanisms, ultimately leading to the malignant transformation of liver cells. Many factors have been identified in the pathogenesis of HBV-associated HCC (HBV-HCC), including HBV gene integration, genomic instability caused by mutation, and activation of cancer-promoting signaling pathways. As research in the progression of HBV-HCC progresses, the role of many new mechanisms, such as epigenetics, exosomes, autophagy, metabolic regulation, and immune suppression, is also being continuously explored. The occurrence of HBV-HCC is a complex process caused by interactions across multiple genes and multiple steps, where the synergistic effects of various cancer-promoting mechanisms accelerate the process of disease evolution from inflammation to tumorigenesis. In this review, we aim to provide a brief overview of the mechanisms involved in the occurrence and development of HBV-HCC, which may contribute to a better understanding of the role of HBV in the occurrence and development of HCC.

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Section: Hbv and Autophagymentioning

confidence: 99%

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

Yu¹,

Han²,

Zhao³

et al. 2021

JHC

115

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“…miR‐155 has been shown to contribute to other processes, including immune and inflammatory reactions, and it was discovered that ectopic miR‐155 expression could eliminate HIV in macrophages arising from monocytes . Sarkar reported that ectopic expression of miR‐155 in HepG2.2.15 cells reduced viral DNA as well as protein titre, and Su reported that miR‐155 enhances innate antiviral immunity through promoting JAK/STAT signalling pathway by targeting SOCS1 and mildly inhibits HBV infection in human hepatoma cells . Our study shows that miR‐155 expression was remarkably inhibited in HepG2 cells transfected with 1.3× copy of an HBV‐containing plasmid, when compared with control cells.…”

Section: Discussionmentioning

confidence: 90%

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Chen

Ming

et al. 2020

Cell Biochemistry & Function

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As small conserved RNAs without a coding function, microRNAs are expressed in multicellular organisms and contribute to the modulation of multiple cellular reactions, such as viral replication, as well as autophagy. microRNAs can regulate host gene expression and inhibit or reinforce hepatitis B virus (HBV) replication. Hepatic cells express miR-155 noticeably. Consequently, our study explored miR-155 modulation of HBV replication and investigated the potential mechanism involved. miR-155 was inhibited on HBV infection. miR-155 transfection remarkably reinforced HBV replication, antigen expression, and progeny secretion in HepG2215 cells. Moreover, miR-155 impaired the inhibition of the cytokine signalling 1 (SOCS1)/Akt/ mTOR axis and reinforced HepG2215 autophagy. Additionally, the autophagy inhibitor (3-MA) eliminated HBsAg secretion triggered by miR-155. Taken together, miR-155 reinforced HBV replication by reinforcing SOCS1-triggered autophagy.Significance of the study: The research studied the potential mechanism involved in HBV replication and miR-155 that miR-155 reinforces HBV replication by reinforcing the SOCS1/Akt/mTOR axis-stimulated autophagy, and therefore, it can provide medical practitioners with the inspiration that chronic HBV might be cured or improved by regulating the activation of miR-155 in cells. In the study, the experiments show that autophagy inhibitors (3-MA) counteracted miR-155 contribution to HBV replication, and it might be a practicable way to improve HBV through some therapies that can repress the autophagy in related cells. K E Y W O R D S autophagy, HBV replication, infection, miR-155, SOCS1

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“…During pregnancy, high concentration of adrenal corticosteroids may in luence the increase in HBV viraemia [11,12]. In most pregnant women with HBV infections and absent HBeAg, viraemia is stable.…”

Section: Discussionmentioning

confidence: 99%

The influence of HBV or HCV infections on the pregnancy course

Łapiński¹

2020

Clin J Obstet Gynecol

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The incidence of HBV infections among the pregnant in Europe falls within the range of 1%-7%, whereas it is 1.7%-4.3% for HCV. The aim was to assess the course of pregnancy among women infected with HBV or HCV, and the condition of neonates in the fi fth minute after the birth. The study included 157 pregnant individuals infected with HBV, 53 infected with HCV, and 330 healthy pregnant women. None of the women infected with HBV and HCV as well as from the control group were infected with HIV, and none of them took intoxicants. Weight of neonates delivered by healthy women was higher as compared with children born by women infected with HBV or HCV (3,517 vs. 3,347 and 3,366). The Apgar score of neonates delivered by women with HBV and HCV infections was lower as compared with the children born by healthy women (9.4 vs. 9.3 vs. 9.7; p < 0.05). Premature births occurred more often in HBV and HCV-infected women than in the control group (14.6% and 24.5% vs. 6.96%; p < 0.05). Miscarriages were signifi cantly more common among the pregnant with HCV infections as compared with the pregnant who were healthy (9.4% vs. 1.8%; p < 0.05). In comparison with the healthy individuals, this group of patients experienced pruritus (10.5% vs. 4.2%; p < 0.05), oedemas (9.4% vs. 2.4%; p < 0.05), and hypertension (9.4% vs. 1.5%; p < 0.05) more often. An increase in HBV loads was observed between the 6th and 28 th-32 nd week of pregnancy among the infected with HBV, and then, a decrease was observed in the 6th months after the delivery. The pregnant infected with HBV without HBsAg (-) and the infected with HCV are subject to common incidence of premature births. Women infected with HCV often experience oedemas, hypertension, and pruritus.

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Dexamethasone Stimulates Hepatitis B Virus (HBV) Replication Through Autophagy

Cited by 21 publications

References 32 publications

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

The Mechanisms of HBV-Induced Hepatocellular Carcinoma

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

The influence of HBV or HCV infections on the pregnancy course

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