Cpg Methylation Participates in Regulation of Hepatitis B Virus Gene Expression in Host Sperm and Sperm-Derived Embryos

Zhong, Chengyao; Lu, Hui; Han, Tae-Ho; Tan, Xiaofang; Li, PengHao; Huang, Jihua; Xie, Qiang; Hou, Zhuoni; Qu, Tingyu; Jiang, Yang; Wang, Sheng; Xu, Lan; Zhong, Ying; Huang, Tian-Hua

doi:10.2217/epi-2016-0129

Cited by 12 publications

(10 citation statements)

References 42 publications

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“…In addition, sperm transcripts are substrates for sperm protein production (Gur and Breitbart 2006;Zhao et al 2009). Recently, HBV gene transcription was confirmed in human spermatozoa and cytosine-phosphorousguanine (CpG) methylation participates in the regulation of HBV gene expression in both host spermatozoa and spermderived embryos (Zhong et al 2017(Zhong et al , 2018. A large-scale investigation of the human sperm proteome has revealed many signalling pathways, including oxidative phosphorylation and oxidative stress pathways (Wang et al 2013).…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus surface protein induces oxidative stress by increasing peroxides and inhibiting antioxidant defences in human spermatozoa

Cheng

Sun

Xie

et al. 2020

Reprod. Fertil. Dev.

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Hepatitis B virus (HBV) infection may affect sperm motility in patients with HBV. HBV surface protein (HBs) decreases mitochondrial membrane potential, impairs motility and induces apoptotic-like changes in human spermatozoa. However, little is known about how human spermatozoa respond to reactive oxygen species (ROS; mainly peroxides) induced by HBs. In this study, HBs induced supraphysiological ROS levels in human spermatozoa and reduced the formation of 2-cell embryos (obtained from hamster oocytes and human spermatozoa). HBs induced a pre-apoptotic status in human spermatozoa, as well as antioxidant defences by increasing glutathione peroxidase 4 (GPX4) and peroxiredoxin 5 (PRDX5) levels. These results highlight the molecular mechanism responsible for the oxidative stress in human spermatozoa exposed to HBV and the antioxidant defence response involving GPX4 and PRDX5.

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Section: Discussionmentioning

confidence: 99%

Hepatitis B virus surface protein induces oxidative stress by increasing peroxides and inhibiting antioxidant defences in human spermatozoa

Cheng

Sun

Xie

et al. 2020

Reprod. Fertil. Dev.

Self Cite

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“…Next, methylation-specific PCR showed that IFN-α did not alter the level of methylation in CpG island II, which regulates the X promoter of HBV cccDNA ( Fig. 2C ) ( 49 ). Bisulfite sequencing also confirmed a similar degree of methylation in CpG island II of HBV cccDNA regardless of interferon treatment (11/52 for control and 13/70 for IFN-α; P=0.723; Fig.…”

Section: Resultsmentioning

confidence: 99%

Methylation profile of hepatitis B virus is not influenced by interferon α in human liver cancer cells

Moon

Kim

2021

Mol Med Rep

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Interferon (IFN) α is used for the treatment of chronic hepatitis B virus (HBV) infection, but the molecular mechanisms underlying its antiviral effect have not been fully elucidated. Epigenetic modifications regulate the transcriptional activity of covalently closed circular DNA (cccDNA) in cells with chronic HBV infection. IFN-α has been shown to modify cccDNA-bound histones, but it is not known whether the anti-HBV effect of IFN-α involves methylation of cccDNA. The present study aimed to determine whether IFN-α induced methylation of HBV cccDNA in a cell-based model in which HepG2 cells were directly infected with wild-type HBV virions. Methylation status of HBV cccDNA was assessed using global DNA methylation ELISA assay, methylation-specific PCR and bisulfite sequencing. IFN-α suppressed HBV DNA and RNA transcripts, but methylation profiles were similar between the control and IFN-α treated groups. Chromatin immunoprecipitation results revealed binding of DNA methyltransferases (DNMT) 3A and DNMT3B to HBV cccDNA and treatment with IFN-α suppressed the recruitment of DNMT3B to cccDNA. Taken together, these results suggest that IFN-α does not induce methylation of HBV cccDNA. Therefore, it was concluded that methylation is unlikely to contribute to the anti-HBV effect of IFN-α in HepG2 cells, and that alternative mechanisms need to be sought to enhance cccDNA methylation as a novel therapy against HBV.

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“…После оплодотворения в цитоплазме ооцита происходит деконденсация хроматина сперматозоида, что имеет большое значение для его активации, и гипометилирование генома эмбриона [26]. Оказалось, что гипометилирование и активация генов ВГВ происходят параллельно с гипометилированием генов эмбриона [27].…”

Section: вирус гепатита вunclassified

Viral infection of spermatozoa. Part 1. Hepatitis B virus and human papillomavirus (review)

Брагина

2021

Androl. genit. hir.

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Intragametal viral infection of spermatozoa can cause true vertical transmission of viruses through germ cells. Currently, human papilloma-virus, including oncogenic risk strains, and hepatitis B virus, have been detected in spermatozoa. The possibility of vertical transmission of hepatitis B virus and human papillomavirus has been proven.Intragametal infection of spermatozoa with viruses of human papillomavirus and hepatitis B virus leads to abnormalities in the development of the embryo and can cause spontaneous abortions both duringnatural conception and when using assisted reproductive technologies.The development of adequate methods for diagnosing an intragametal spermatozoa virus infection will make it possible to find out, at least in some patients, the cause of infertility and pregnancy abnormalities and apply appropriate antiviral therapy in preparation for natural conception or the use of assisted reproductive technologies.

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Cpg Methylation Participates in Regulation of Hepatitis B Virus Gene Expression in Host Sperm and Sperm-Derived Embryos

Abstract: HBV CpG sites can be methylated in patient sperm before maturation. Methylation of CpG islands II and III participates in transcriptional regulation of HBV X and S genes, respectively, in sperm and sperm-derived embryos.

Cited by 12 publications

References 42 publications

Hepatitis B virus surface protein induces oxidative stress by increasing peroxides and inhibiting antioxidant defences in human spermatozoa

Hepatitis B virus surface protein induces oxidative stress by increasing peroxides and inhibiting antioxidant defences in human spermatozoa

Methylation profile of hepatitis B virus is not influenced by interferon α in human liver cancer cells

Viral infection of spermatozoa. Part 1. Hepatitis B virus and human papillomavirus (review)

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