Research ExplorerPublicationsEpigenetic modulation in chronic hepatitis B virus infection

Epigenetic modulation in chronic hepatitis B virus infection

Standard

Epigenetic modulation in chronic hepatitis B virus infection. / Dandri, Maura.

In: SEMIN IMMUNOPATHOL, Vol. 42, No. 2, 04.2020, p. 173-185.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Dandri, M 2020, 'Epigenetic modulation in chronic hepatitis B virus infection', SEMIN IMMUNOPATHOL, vol. 42, no. 2, pp. 173-185. https://doi.org/10.1007/s00281-020-00780-6

APA

Dandri, M. (2020). Epigenetic modulation in chronic hepatitis B virus infection. SEMIN IMMUNOPATHOL, 42(2), 173-185. https://doi.org/10.1007/s00281-020-00780-6

Vancouver

Dandri M. Epigenetic modulation in chronic hepatitis B virus infection. SEMIN IMMUNOPATHOL. 2020 Apr;42(2):173-185. https://doi.org/10.1007/s00281-020-00780-6

Bibtex

@article{0f476051b9284eb7ad9780d4c4e17085,
title = "Epigenetic modulation in chronic hepatitis B virus infection",
abstract = "The human hepatitis B virus (HBV) is a small-enveloped DNA virus causing acute and chronic hepatitis. Despite the existence of an effective prophylactic vaccine and the strong capacity of approved antiviral drugs to suppress viral replication, chronic HBV infection (CHB) continues to be a major health burden worldwide. Both the inability of the immune system to resolve CHB and the unique replication strategy employed by HBV, which forms a stable viral covalently closed circular DNA (cccDNA) minichromosome in the hepatocyte nucleus, enable infection persistence. Knowledge of the complex network of interactions that HBV engages with its host is still limited but accumulating evidence indicates that epigenetic modifications occurring both on the cccDNA and on the host genome in the course of infection are essential to modulate viral activity and likely contribute to pathogenesis and cancer development. Thus, a deeper understanding of epigenetic regulatory processes may open new venues to control and eventually cure CHB. This review summarizes major findings in HBV epigenetic research, focusing on the epigenetic mechanisms regulating cccDNA activity and the modifications determined in infected host cells and tumor liver tissues.",
author = "Maura Dandri",
year = "2020",
month = apr,
doi = "10.1007/s00281-020-00780-6",
language = "English",
volume = "42",
pages = "173--185",
journal = "SEMIN IMMUNOPATHOL",
issn = "1863-2297",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - Epigenetic modulation in chronic hepatitis B virus infection

AU - Dandri, Maura

PY - 2020/4

Y1 - 2020/4

N2 - The human hepatitis B virus (HBV) is a small-enveloped DNA virus causing acute and chronic hepatitis. Despite the existence of an effective prophylactic vaccine and the strong capacity of approved antiviral drugs to suppress viral replication, chronic HBV infection (CHB) continues to be a major health burden worldwide. Both the inability of the immune system to resolve CHB and the unique replication strategy employed by HBV, which forms a stable viral covalently closed circular DNA (cccDNA) minichromosome in the hepatocyte nucleus, enable infection persistence. Knowledge of the complex network of interactions that HBV engages with its host is still limited but accumulating evidence indicates that epigenetic modifications occurring both on the cccDNA and on the host genome in the course of infection are essential to modulate viral activity and likely contribute to pathogenesis and cancer development. Thus, a deeper understanding of epigenetic regulatory processes may open new venues to control and eventually cure CHB. This review summarizes major findings in HBV epigenetic research, focusing on the epigenetic mechanisms regulating cccDNA activity and the modifications determined in infected host cells and tumor liver tissues.

AB - The human hepatitis B virus (HBV) is a small-enveloped DNA virus causing acute and chronic hepatitis. Despite the existence of an effective prophylactic vaccine and the strong capacity of approved antiviral drugs to suppress viral replication, chronic HBV infection (CHB) continues to be a major health burden worldwide. Both the inability of the immune system to resolve CHB and the unique replication strategy employed by HBV, which forms a stable viral covalently closed circular DNA (cccDNA) minichromosome in the hepatocyte nucleus, enable infection persistence. Knowledge of the complex network of interactions that HBV engages with its host is still limited but accumulating evidence indicates that epigenetic modifications occurring both on the cccDNA and on the host genome in the course of infection are essential to modulate viral activity and likely contribute to pathogenesis and cancer development. Thus, a deeper understanding of epigenetic regulatory processes may open new venues to control and eventually cure CHB. This review summarizes major findings in HBV epigenetic research, focusing on the epigenetic mechanisms regulating cccDNA activity and the modifications determined in infected host cells and tumor liver tissues.

U2 - 10.1007/s00281-020-00780-6

DO - 10.1007/s00281-020-00780-6

M3 - SCORING: Review article

C2 - 32185454

VL - 42

SP - 173

EP - 185

JO - SEMIN IMMUNOPATHOL

JF - SEMIN IMMUNOPATHOL

SN - 1863-2297

IS - 2

ER -