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Epigenetic Regulation of Hepatitis B...

University of Illinois at Chicago.

Epigenetic Regulation of Hepatitis B Virus In Vivo /

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Epigenetic Regulation of Hepatitis B Virus In Vivo // Rachel Matrenec Collopy.
作者:	Collopy, Rachel Matrenec,
面頁冊數:	1 electronic resource (106 pages)
附註:	Source: Dissertations Abstracts International, Volume: 86-04, Section: B.
提要註:	Chronic hepatitis B virus (HBV) infection is a global public health concern responsible for nearly 1 million deaths annually. Current mainstays of HBV treatment, nucleoside analogs and interferon, are associated with drug resistance and negative side effects. Most importantly, these treatments are not curative and only slow the progression of chronic HBV, which frequently leads to significant liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Chronic HBV infection is maintained by viral covalently closed circular (ccc) DNA, a highly stable replication product and transcriptional template which exists as an episome in the nucleus. As such, the epigenetic silencing of nuclear HBV DNA represents one potential mechanism that may address curing chronic HBV infection. The limited coding capacity of the virus leaves few viral drug targets. As such, targeting host cellular factors that contribute to successful HBV replication is imperative. This current study explores the roles of Foxa and Ten-eleven translocation (Tet) methylcytosine dioxygenases in the epigenetic regulation of HBV DNA.Liver-specific Foxa- and Tet-deficient HBV transgenic mice are useful in vivo models of chronic HBV infection. HBV cccDNA is associated with histones and assembled into chromatin in patients. It is likely subject to regulation similar to that of the HBV transgene in this mouse model. Liver-specific Foxa-deficient HBV transgenic mice do not replicate HBV due to the specific transcriptional silencing of the viral DNA as a result of methylation. The methylation of the HBV DNA is observed in these mice regardless of which Foxa factor is deleted, suggesting that the level of Foxa factor activity governs the demethylation of the HBV transgene, rather than the expression of any specific Foxa factor. Similarly, Tet-deficient HBV transgenic mice display high levels of viral DNA methylation and very low levels of viral transcription and replication. Together, these observations suggest that Foxa and/or Tet enzymes are viable drug targets that may offer resolution of chronic HBV infection.
Contained By:	Dissertations Abstracts International86-04B.
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31693775
ISBN:	9798384461111

Epigenetic Regulation of Hepatitis B Virus In Vivo /
Collopy, Rachel Matrenec,

Epigenetic Regulation of Hepatitis B Virus In Vivo /Rachel Matrenec Collopy. - 1 electronic resource (106 pages)

Source: Dissertations Abstracts International, Volume: 86-04, Section: B.

Chronic hepatitis B virus (HBV) infection is a global public health concern responsible for nearly 1 million deaths annually. Current mainstays of HBV treatment, nucleoside analogs and interferon, are associated with drug resistance and negative side effects. Most importantly, these treatments are not curative and only slow the progression of chronic HBV, which frequently leads to significant liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Chronic HBV infection is maintained by viral covalently closed circular (ccc) DNA, a highly stable replication product and transcriptional template which exists as an episome in the nucleus. As such, the epigenetic silencing of nuclear HBV DNA represents one potential mechanism that may address curing chronic HBV infection. The limited coding capacity of the virus leaves few viral drug targets. As such, targeting host cellular factors that contribute to successful HBV replication is imperative. This current study explores the roles of Foxa and Ten-eleven translocation (Tet) methylcytosine dioxygenases in the epigenetic regulation of HBV DNA.Liver-specific Foxa- and Tet-deficient HBV transgenic mice are useful in vivo models of chronic HBV infection. HBV cccDNA is associated with histones and assembled into chromatin in patients. It is likely subject to regulation similar to that of the HBV transgene in this mouse model. Liver-specific Foxa-deficient HBV transgenic mice do not replicate HBV due to the specific transcriptional silencing of the viral DNA as a result of methylation. The methylation of the HBV DNA is observed in these mice regardless of which Foxa factor is deleted, suggesting that the level of Foxa factor activity governs the demethylation of the HBV transgene, rather than the expression of any specific Foxa factor. Similarly, Tet-deficient HBV transgenic mice display high levels of viral DNA methylation and very low levels of viral transcription and replication. Together, these observations suggest that Foxa and/or Tet enzymes are viable drug targets that may offer resolution of chronic HBV infection.

English

ISBN: 9798384461111Subjects--Topical Terms:

187040
Immunology.
Subjects--Index Terms:

Hepatitis B virus

Epigenetic Regulation of Hepatitis B Virus In Vivo /
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520 $a Chronic hepatitis B virus (HBV) infection is a global public health concern responsible for nearly 1 million deaths annually. Current mainstays of HBV treatment, nucleoside analogs and interferon, are associated with drug resistance and negative side effects. Most importantly, these treatments are not curative and only slow the progression of chronic HBV, which frequently leads to significant liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Chronic HBV infection is maintained by viral covalently closed circular (ccc) DNA, a highly stable replication product and transcriptional template which exists as an episome in the nucleus. As such, the epigenetic silencing of nuclear HBV DNA represents one potential mechanism that may address curing chronic HBV infection. The limited coding capacity of the virus leaves few viral drug targets. As such, targeting host cellular factors that contribute to successful HBV replication is imperative. This current study explores the roles of Foxa and Ten-eleven translocation (Tet) methylcytosine dioxygenases in the epigenetic regulation of HBV DNA.Liver-specific Foxa- and Tet-deficient HBV transgenic mice are useful in vivo models of chronic HBV infection. HBV cccDNA is associated with histones and assembled into chromatin in patients. It is likely subject to regulation similar to that of the HBV transgene in this mouse model. Liver-specific Foxa-deficient HBV transgenic mice do not replicate HBV due to the specific transcriptional silencing of the viral DNA as a result of methylation. The methylation of the HBV DNA is observed in these mice regardless of which Foxa factor is deleted, suggesting that the level of Foxa factor activity governs the demethylation of the HBV transgene, rather than the expression of any specific Foxa factor. Similarly, Tet-deficient HBV transgenic mice display high levels of viral DNA methylation and very low levels of viral transcription and replication. Together, these observations suggest that Foxa and/or Tet enzymes are viable drug targets that may offer resolution of chronic HBV infection.
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653 $a Epigenetic modification
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