Mother-to-child transmission of hepatitis B virus: Evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era

Li, Zixiong; Xie, Zhenyu; Ni, Hongxia; Zhang, Qi; Lu, Wei; Yin, Jianhua; Liu, Wenbin; Ding, Yibo; Zhao, Yan; Zhu, Yongxian; Pu, Rui; Zhang, Hongwei; Dong, Hongjun; Fu, Yifei; Sun, Qiang; Xu, Guozhang; Cao, Guangwen

doi:10.1016/j.jcv.2014.06.010

Cited by 33 publications

(48 citation statements)

References 34 publications

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“…During chronic HBV infection, the HCC-risk HBV mutations, including A1762T/G1764A, C1653T, and T1753V, accumulate consecutively before HCC occurrence. A1762T/G1764A is an earlier generated HCC-risk mutation, whereas C1653T and T1753V are later generated ones (25,31,34). Furthermore, HBV combo mutations have higher specificities than single ones in indicating HCC (24,25).…”

Section: Discussionmentioning

confidence: 97%

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Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Yin

Wang

et al. 2015

Cancer Prevention Research

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We aimed to evaluate whether hepatitis B virus (HBV) mutations at the core promoter region could improve the prediction and specific prophylaxis of hepatocellular carcinoma (HCC) in chronic HBV-infected patients. A total of 2,114 HBV-infected patients enrolled between August 1998 and December 2007 were followed-up for 18,406 person-years. Of those, 612 received !48 week treatments with nucleos(t)ide analogue (NA) and/or IFNa.

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Section: Discussionmentioning

confidence: 97%

“…The core promoter region from nt.1626 to nt.2004 of HBV genome was amplified using nested PCR and directly sequenced or sequenced after cloning (25,31). The sequences were aligned and analyzed using MEGA5.0 and Bioedit 7.0 software packages and deposited in GenBank with accession numbers KF164837-KF166793.…”

Section: Hbv Genotyping and Mutation Assaymentioning

confidence: 99%

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Yin

Wang

et al. 2015

Cancer Prevention Research

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“…Several longitudinal studies carried in China have also demonstrated that baseline A1762T/G1764A mutation increases the risk of HCC in chronic HBV carriers or CHB patients [34][35][36][37] . Among the HCC-risk HBV mutations, the A1762T/G1764A is usually detected in the early stage in young adolescents, while other mutations including T1753V, C1653T, G1899A, and preS deletion appear only at the late stage of chronic HBV infection [12,38] . Reaction to chronic HBV infection, as characterized by immune response-induced hepatocyte damage and release of transaminase, facilitates the generation of the HBV mutations, indicating active immune selection of the HBV mutants during HBeAg seroconversion from HBeAg-positive to HBeAg-negative.…”

Section: "Dead-end" Evolution Of Hbvmentioning

confidence: 99%

“…HBV that has a low density of CD8 + T cell epitope in their core and X proteins are selected during long-term evolution [39] , thus CD8 + T cells play an important role in the immune selection of HCC-related HBV mutants [ Figure 2]. HBV acquired during infancy or early childhood, or at early infection stage in adults, is usually in the form of wild-type [12,38] . In the initial immune tolerant phase of chronic HBV infection, HBeAg is positive, viral load is high, and immune pressure is weak.…”

Section: Reduction Of Cd8mentioning

confidence: 99%

“…In the HBV-infected children, the frequencies and locations of HCC-related mutations increase with increasing age. However, compared with their mothers who have been exposed to chronic infection for approximately 25 years, children have fewer HCCrelated HBV mutations [38] . In individuals with chronic HBV infection, HBV is synthesized and packaged in hepatocytes and released into the circulation at a pace of up to 1011 viral particles daily.…”

Section: Reduction Of Cd8mentioning

confidence: 99%

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Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

Cao¹

2017

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How to cite this article: Cao GW. Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis. Hepatoma Res 2017;3:241-59.Non-resolving inflammation, which may be maintained by infection, pollution, and metabolic stimulants and their interactions with immunogenetic predisposition, provides a fertile field for cancer development. This is strongly evident in hepatocellular carcinoma. Here, the framework of a hypothesis called Cancer Evo-Dev is presented, based on the advances in hepatitis B virusinduced hepatocarcinogenesis. Several aspects central to this theory are as follows: (1) immune imbalance caused by the interaction of immunogenetic predispositions and hepatitis B virus infection maintains non-resolving inflammation; (2) active inflammation executants promote mutations in viral and host genomes via disbalancing mutagenic forces including cytidine deaminases and mutation-repairing forces including uracil-DNA glycosylases, thus promoting cancer-related somatic mutations and viral mutations; (3) a small percentage of the cells whose somatic mutations alter the survival signalling adapt to the inflammatory microenvironment, de-differentiate via demethylating role of cytidine deaminases, and reversely develop into tumor-initiating cells (TICs); (4) under the cultivation of some factors like POSTN from tumorinfiltrating fibroblasts and M2 macrophages, TICs acquire the stemness, cancer-stem cells obtain distinct metastatic and drug-resistant potentials under the selection pressure from distinct microenvironments; (5) glycolysis persistence in the presence of oxygen provides essential energy for cell survival and the raw material for DNA synthesis. Thus, cancer development is characterized by an evolutionary process of "mutation-selection-adaptation". The framework of Cancer Evo-Dev can be verified in other cancers. Cancer Evo-Dev lays theoretical foundation for understanding the mechanisms by which inflammation promotes cancer development, and it also plays a role in specific prophylaxis, prediction, and targeted treatment of cancers. Key words:Inflammation, hepatitis B virus, mutations, hepatoma, Cancer Evo-Dev ABSTRACTArticle history:

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Hepatitis Viruses and Hepatoma

Wang¹,

Cao

et al. 2017

Holland‐Frei Cancer Medicine

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Overview Hepatitis is an inflammation of the liver, occurring as the result of a viral infection or the exposure of liver to toxic substances such as alcohol or aflatoxin B. Hepatitis viruses are the most common cause of hepatitis in the world, of which HBV and HCV can cause persistent liver infection, frequently resulting in chronic hepatitis, liver cirrhosis, and eventually hepatocellular carcinoma (HCC). HBV belongs to the genus Orthohepadnavirus of the Hepadnaviridae with a circular incomplete double‐stranded DNA genome, containing four overlapping open reading frames (ORFs) that encode the surface envelope protein (HBsAg), the core protein (HBcAg and HBeAg), a polymerase, and a multifunctional nonstructural protein termed X (HBx), respectively. HBV genotypes and subgenotypes have distinct geographical distributions. In East Asia, HBV genotypes B and C are endemic. Accordingly, any differences in its global incidence may be explained by differences in the HCV and HBV prevalence. It has been estimated that 57% of cirrhosis is attributable to either HBV (30%) or HCV (27%) and 78% of HCC is attributable to HBV (53%) or HCV (25%). In China, up to 80% of HCC cases are attributable to HBV, and approximately 20% of HCC patients test positive for HCV‐RNA. Besides the oncogenic function of HBV‐encoding protein, the HBV infection‐induced virus or host DNA mutation has been found contribution for HCC development. Unlike to HBV, HCV belongs to the genus Hepacivirus of the Flaviviridae family, with a single‐stranded positive‐sense RNA genome. There is no host genome integration, nor does HCV contain any known oncogenes. The major mechanisms of HCV‐induced hepatocarcinogenesis include the oncogenic effect of HCV viral proteins, steatosis and insulin resistance, chronic inflammation and fibrosis, oxidative stress, and chromosomal instability. This chapter exclusively focuses on hepatitis and hepatoma caused mainly by HBV and HCV infection, discussing epidemiologic considerations, construction and genotype, role of virus in performing HCC, and early diagnosis and prophylaxis. Still, viruses that selectively infect endemic host predispose patients to malignant hepatoma, to some extent, placing a burden on the healthcare worldwide. Therefore, an upturn in morbidity of hepatitis and hepatoma will be of great importance in public health.

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Mother-to-child transmission of hepatitis B virus: Evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era

Cited by 33 publications

References 34 publications

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

Hepatitis Viruses and Hepatoma

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