Adenovirus vector encoding TPPII ignites HBV‐specific CTL response by activating autophagy in CD8+ T cell

Tan, Quanhui; Jie, Chen; Gao, Gao; YiZhang,; Chen, Xiaohua; Yu, Yongsheng; Guo-qin, Zang; Tang, Zhenghao

doi:10.1111/jvh.13638

Cited by 3 publications

(5 citation statements)

References 35 publications

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“…Autophagy and tripeptidyl peptidase II (TPPII) are associated with HBV infection. Tan's study showed that adenovirus vector-HBcAg-TPPII promotes autophagy of CD8 + T cells, and inhibits HBV DNA replication and HBsAg expression in HBV transgenic mice, and elucidated that the PI3K/AKT signaling pathway may be involved in this autophagy process, and this theoretical basis provides a potential candidate for HBV immunotherapy (Tan et al, 2021). A similar effect was found on immature dendritic cells (imDCs) stimulated by nicotine.…”

Section: Therapeutics That Modulate Pi3k/ Akt Signaling Pathways To C...mentioning

confidence: 82%

Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection

Yan

Qiu

Davgadorj

et al. 2022

Front. Cell. Infect. Microbiol.

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Numerous canonical cellular signaling pathways modulate hepatitis B virus (HBV) replication. HBV genome products are known to play a significant role in regulating these cellular pathways for the liver’s viral-related pathology and physiology and have been identified as the main factor in hepatocarcinogenesis. Signaling changes during viral replication ultimately affect cellular persistence, multiplication, migration, genome instability, and genome damage, leading to proliferation, evasion of apoptosis, block of differentiation, and immortality. Recent studies have documented that numerous signaling pathway agonists or inhibitors play an important role in reducing HBV replication in vitro and in vivo, and some have been used in phase I or phase II clinical trials. These optional agents as molecular therapeutics target cellular pathways that could limit the replication and transcription of HBV or inhibit the secretion of the small surface antigen of HBV in a signaling-independent manner. As principle-based available information, a combined strategy including antiviral therapy and immunomodulation will be needed to control HBV infection effectively. In this review, we summarize recent findings on interventions of molecular regulators in viral replication and the interactions of HBV proteins with the components of the various targeting cellular pathways, which may assist in designing novel agents to modulate signaling pathways to prevent HBV replication or carcinogenesis.

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Section: Therapeutics That Modulate Pi3k/ Akt Signaling Pathways To C...mentioning

confidence: 82%

Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection

Yan

Qiu

Davgadorj

et al. 2022

Front. Cell. Infect. Microbiol.

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“…43 However, accumulating evidences indicated that HBV could not only induce the formation of autophagy but also induce incomplete autophagy by damaging lysosome acidification and promote self-replication. 44 On the other hand, EGCG treatment neutralizes incomplete autophagy caused by HBV through the promotion of lysosomal acidification, which is detrimental to HBV replication. 45 Therefore, increasing lysosomal acidification to repair its degradative capacity may be a promising strategy.…”

Section: Discussionmentioning

confidence: 99%

“…Also, autophagy negatively regulated the replication of HCV in the presence of IFNs . However, accumulating evidences indicated that HBV could not only induce the formation of autophagy but also induce incomplete autophagy by damaging lysosome acidification and promote self-replication . On the other hand, EGCG treatment neutralizes incomplete autophagy caused by HBV through the promotion of lysosomal acidification, which is detrimental to HBV replication .…”

Section: Discussionmentioning

confidence: 99%

Tannic Acid Suppresses HBV Replication via the Regulation of NF-κB, MAPKs, and Autophagy in HepG2.2.15 Cells

Wang

Zhou

Yin

et al. 2023

J. Agric. Food Chem.

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Hepatitis B virus (HBV) infection is a serious global health problem that threatens the health of human. Tannic acid (TA), a natural polyphenol in foods, fruits, and plants, exhibits a variety of bioactive functions. In our research, we decide to explore the pharmacological mechanism of TA against HBV replication. Our results showed that TA effectively reduced the content of HBV DNA and viral antigens (HBsAg and HBeAg) in HepG2.2.15 cells. Meanwhile, TA significantly decreased the mRNA expression of HBV RNA, which include total HBV RNA, HBV pregenomic RNA, and HBV precore mRNA. Besides, TA evidently downregulated the activity of HBV promoters in HepG2.2.15 cells. Furthermore, we found that TA upregulated the expression of IL-8, TNF-α, IFN-α, and IFN-α-mediated antiviral effectors in HepG2.2.15 cells. On the contrary, TA downregulated the expression of IL-10 and hepatic nuclear factor 4 (HNF4α). In addition, TA activated the NF-κB and MAPK pathways that contributed to the inhibition of HBV replication. Finally, TA treatment led to the occurrence of autophagy, which accelerated the elimination of HBV components in HepG2.2.15 cells. Taken together, our results elucidated the suppressive effect of TA on HBV replication and provided inspiration for its clinical application in HBV treatment.

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“…Autophagy plays a paramount role in health and disease and was first proposed by Belgian scientist Christian de Duve in 1963 21–23 . Currently, increasing evidence demonstrates that autophagy is involved in HBV replication and liver cancer migration and invasion 24,25 . In vitro studies have demonstrated that ATG5 gene knockout reduces HBV gene expression 26 and may facilitate the development of liver and lung tumors 27,28 .…”

Section: Discussionmentioning

confidence: 99%

“…[21][22][23] Currently, increasing evidence demonstrates that autophagy is involved in HBV replication and liver cancer migration and invasion. 24,25 In vitro studies have demonstrated that ATG5 gene knockout reduces HBV gene expression 26 and may facilitate the development of liver and lung tumors. 27,28 In addition, ATG16L1 proteins were upregulated in HBV-related HCC compared to adjacent nontumor tissues.…”

Section: Discussionmentioning

confidence: 99%

Association of ATG16L1 and ATG5 gene polymorphisms with susceptibility to hepatitis B virus infection and progression to HCC in central China

Wu,

Ouyang

2023

Microbiology and Immunology

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Hepatitis B virus (HBV) infection is a severe public health problem worldwide. The relationship between polymorphisms of autophagy‐related 16‐like 1 gene (ATG16L1) and autophagy‐related gene 5 (ATG5) with susceptibility to the stage of HBV infection has been reported in different populations. Nevertheless, this association is not seen in the population of central China. This study recruited 452 participants, including 246 HBV‐infected patients (139 chronically infected HBV without hepatocellular carcinoma [HCC] and 107 HBV‐related HCC patients) and 206 healthy controls. Genotyping of ATG16L1 rs2241880 and ATG5 rs688810 were performed using Sanger sequencing and polymerase chain reaction‐restriction fragment length polymorphism, respectively. Our results indicated that the G allele of ATG16L1 rs2241880 was more frequent in healthy controls than in patients with chronicHBV infection. After adjusting for age and sex, an association between the ATG16L1 rs2241880 polymorphism and HBV infection was significant under the dominant and allele models (p = 0.009 and 0.003, respectively). However, no association between the ATG5 polymorphisms and HBV infection was observed. We also did not find a significant association between ATG16L1 and ATG5 polymorphisms and the progression of HBV‐related HCC. Therefore, the genetic polymorphism of ATG16L1 rs2241880 may be associated with susceptibility to HBV infection in the population of central China.

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Adenovirus vector encoding TPPII ignites HBV‐specific CTL response by activating autophagy in CD8+ T cell

Cited by 3 publications

References 35 publications

Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection

Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection

Tannic Acid Suppresses HBV Replication via the Regulation of NF-κB, MAPKs, and Autophagy in HepG2.2.15 Cells

Association of ATG16L1 and ATG5 gene polymorphisms with susceptibility to hepatitis B virus infection and progression to HCC in central China

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