Interferon and interferon-stimulated genes in HBV treatment

Li, Qirong; Sun, Baozhen; Yang, Zhuo; Jiang, Ziping; Li, Rong; Lin, Cheng‐Fang; Jin, Yongfeng; Gao, Yongjian; Wang, Dongxu

doi:10.3389/fimmu.2022.1034968

Cited by 29 publications

(28 citation statements)

References 135 publications

(149 reference statements)

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“…ISGs are the main anti-viral factors of the host and also causative agent in treatment of HBV patients ( Li et al., 2022 ). Genetic polymorphisms of the ISG genes have been associated with HBV infection, disease progression, and outcome in HBV patients.…”

Section: Discussionmentioning

confidence: 99%

Association of genetic polymorphisms in the C19orf66 gene and biochemical indices of HBV infected individuals in Yunnan

Liu

Yang

et al. 2023

Front. Cell. Infect. Microbiol.

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IntroductionHepatitis B virus (HBV) infection causes serious liver diseases and is a healthy problem worldwide. Although vaccines are administered to infants after birth, there is no effective medicine for HBV infection. The interferon-stimulated genes (ISGs) are important factors in the host that can aid in restraining the virus, and the C19orf66 gene has a wide-antiviral spectrum.MethodsIn this study, three SNPs in the C19orf66 gene were sequenced and genotyped, and their potential function were predicted and further verified by dual-luciferase reporter assay.ResultsAlthough no significant difference of genotype and allele frequency was observed between HBV patients and the controls, the genotype and allele frequency showed significant difference between HBV patients with HBsAg-positive and HBV patients with HBsAg-negative or controls. Genotype AA (P= 0.009) and AT (P= 0.019) of rs77076061 showed higher and lower frequency in HBV patients with HBsAg-positive than in patients with HBsAg-negative, respectively. Genotype AG of rs1979262 played a risk role in HBV patients with HBsAg-positive (13.22%) than in patients with HBsAg-negative (7.53%, P= 0.036) or controls (8.48%, P= 0.033). The frequency of allele A of rs1979262 was higher in patients with HBsAg-positive (6.61%) than in patients with HBsAg-negative (3.77%, P= 0.042), while it was the opposite for the allele G. Moreover, the associations between genotypes of SNPs in the C19orf66 gene and the ALT, AST, and DBIL level were also identified. The functional assay suggested that the SNPs might influence the C19orf66 expression by changing the connection of transcriptional factors.ConclusionIn summary, the association between genetic polymorphisms in the C19orf66 gene and HBV infection/biochemical indices of patients was firstly identified in Yunnan Province.

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Section: Discussionmentioning

confidence: 99%

Association of genetic polymorphisms in the C19orf66 gene and biochemical indices of HBV infected individuals in Yunnan

Liu

Yang

et al. 2023

Front. Cell. Infect. Microbiol.

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“…IFNs are essential for HBV transcription and replication through the induction of IFN-stimulated genes (ISGs). 29 For example, APOBEC3A was activated by IFNα and prevented HBV replication by reducing the transcription of pgRNA and subgenomic RNA. 26 Sajid et al 30 reported that IFN-a-inducible protein 6 restricted HBV replication by decreasing the level of HBV enhancer II and core promoter (EnhII/Cp) genes.…”

Section: Discussionmentioning

confidence: 99%

“…IFNs are essential for HBV transcription and replication through the induction of IFN‐stimulated genes (ISGs) 29 . For example, APOBEC3A was activated by IFNα and prevented HBV replication by reducing the transcription of pgRNA and subgenomic RNA 26 .…”

Section: Discussionmentioning

confidence: 99%

Higher BST2 Expression Promotes the Anti‐HBV Effect of IFN‐α and BST2 Genetic Variant Predicts PegIFNα Treatment Response of HBeAg‐Positive Chronic Hepatitis B Patients

Chen,

Hou,

et al. 2023

Clin Pharma and Therapeutics

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We previously reported that an interferon (IFN)‐inducible protein, BST2, was regulated by the JAK–STAT pathway activated by CD40, and subsequently suppressing hepatitis B virus (HBV) repliaction and transcription. The current research attempted to assess the impact of BST2 on the IFN‐treated anti‐HBV effect, and explore BST2 variants for predicting pegylated IFN alpha (PegIFNα) therapy response of patients with hepatitis B e antigen (HBeAg)‐positive chronic hepatitis B (CHB). Using an HBV‐transfected cell model, the function of BST2 on HBV DNA replication and transcription driven by IFN was studied. The potentially functional BST2 variants were selected through a strategy of gene‐wide screening. The associations of BST2 variants and polygenic score (PGS) model, which was used to quantify the combined influence of several genetic variants, with treatment response were examined in 2 separate PegIFNα‐treated cohorts of 238 and 707 patients with CHB, respectively. We found that overexpression of BST2 improved the anti‐HBV activity triggered by IFN‐α. Among PegIFNα‐treated patients with CHB, BST2_rs9576 was screened out to be significantly correlated with combined response (CR; i.e., HBeAg seroconversion along with HBV DNA level <3.3log10IU/mL, P = 7.12 × 10−5). Additionally, there was a strong correlation between the PGS incorporating BST2_rs9576 and other 5 genetic variations (previously described predictors of therapy response to PegIFNα) and CR (P = 1.81 × 10−13), hepatitis B surface antigen (HBsAg) level (P = 0.004), as well as HBsAg decline (P = 0.017). In conclusion, higher BST2 expression responded better to IFN‐α treatment. BST2_rs9576 is an effective indicator to forecast therapy response of PegIFNα‐treated patients with CHB. The PGS possesses the potential to boost the ability of PegIFNα therapy response.

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“…On the one hand, the IFN-mediated antiviral response mainly includes type I and type IIIFN responses [ 122 ]. To our knowledge, TRLs play an essential role in the IFN-mediated innate host antiviral response.…”

Section: Antivirals Against Jev Infectionmentioning

confidence: 99%

Recent Advances in Antivirals for Japanese Encephalitis Virus

Zhu

Chen

Lurong

et al. 2023

Viruses

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Culex mosquitoes are the primary vectors of the Japanese encephalitis virus (JEV). Since its discovery in 1935, Japanese encephalitis (JE), caused by JEV, has posed a significant threat to human health. Despite the widespread implementation of several JEV vaccines, the transmission chain of JEV in the natural ecosystem has not changed, and the vector of transmission cannot be eradicated. Therefore, JEV is still the focus of attention for flaviviruses. At present, there is no clinically specific drug for JE treatment. JEV infection is a complex interaction between the virus and the host cell, which is the focus of drug design and development. An overview of antivirals that target JEV elements and host factors is presented in this review. In addition, drugs that balance antiviral effects and host protection by regulating innate immunity, inflammation, apoptosis, or necrosis are reviewed to treat JE effectively.

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Interferon and interferon-stimulated genes in HBV treatment

Cited by 29 publications

References 135 publications

Association of genetic polymorphisms in the C19orf66 gene and biochemical indices of HBV infected individuals in Yunnan

Association of genetic polymorphisms in the C19orf66 gene and biochemical indices of HBV infected individuals in Yunnan

Higher BST2 Expression Promotes the Anti‐HBV Effect of IFN‐α and BST2 Genetic Variant Predicts PegIFNα Treatment Response of HBeAg‐Positive Chronic Hepatitis B Patients

Recent Advances in Antivirals for Japanese Encephalitis Virus

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