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CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X

Standard

CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X. / Karimova, Madina; Beschorner, Niklas; Dammermann, Werner; Chemnitz, Jan; Indenbirken, Daniela; Bockmann, Jan-Hendrik; Grundhoff, Adam; Lüth, Stefan; Buchholz, Frank; Schulze zur Wiesch, Julian; Hauber, Joachim.

in: SCI REP-UK, Jahrgang 5, 03.09.2015, S. 13734.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Karimova, M, Beschorner, N, Dammermann, W, Chemnitz, J, Indenbirken, D, Bockmann, J-H, Grundhoff, A, Lüth, S, Buchholz, F, Schulze zur Wiesch, J & Hauber, J 2015, 'CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X', SCI REP-UK, Jg. 5, S. 13734. https://doi.org/10.1038/srep13734

APA

Karimova, M., Beschorner, N., Dammermann, W., Chemnitz, J., Indenbirken, D., Bockmann, J-H., Grundhoff, A., Lüth, S., Buchholz, F., Schulze zur Wiesch, J., & Hauber, J. (2015). CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X. SCI REP-UK, 5, 13734. https://doi.org/10.1038/srep13734

Vancouver

Karimova M, Beschorner N, Dammermann W, Chemnitz J, Indenbirken D, Bockmann J-H et al. CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X. SCI REP-UK. 2015 Sep 3;5:13734. https://doi.org/10.1038/srep13734

Bibtex

@article{a36f8e5b9adf41f3aa598b3101f11c5f,
title = "CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X",
abstract = "Current antiviral therapies cannot cure hepatitis B virus (HBV) infection; successful HBV eradication would require inactivation of the viral genome, which primarily persists in host cells as episomal covalently closed circular DNA (cccDNA) and, to a lesser extent, as chromosomally integrated sequences. However, novel designer enzymes, such as the CRISPR/Cas9 RNA-guided nuclease system, provide technologies for developing advanced therapy strategies that could directly attack the HBV genome. For therapeutic application in humans, such designer nucleases should recognize various HBV genotypes and cause minimal off-target effects. Here, we identified cross-genotype conserved HBV sequences in the S and X region of the HBV genome that were targeted for specific and effective cleavage by a Cas9 nickase. This approach disrupted not only episomal cccDNA and chromosomally integrated HBV target sites in reporter cell lines, but also HBV replication in chronically and de novo infected hepatoma cell lines. Our data demonstrate the feasibility of using the CRISPR/Cas9 nickase system for novel therapy strategies aiming to cure HBV infection.",
author = "Madina Karimova and Niklas Beschorner and Werner Dammermann and Jan Chemnitz and Daniela Indenbirken and Jan-Hendrik Bockmann and Adam Grundhoff and Stefan L{\"u}th and Frank Buchholz and {Schulze zur Wiesch}, Julian and Joachim Hauber",
year = "2015",
month = sep,
day = "3",
doi = "10.1038/srep13734",
language = "English",
volume = "5",
pages = "13734",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - CRISPR/Cas9 nickase-mediated disruption of hepatitis B virus open reading frame S and X

AU - Karimova, Madina

AU - Beschorner, Niklas

AU - Dammermann, Werner

AU - Chemnitz, Jan

AU - Indenbirken, Daniela

AU - Bockmann, Jan-Hendrik

AU - Grundhoff, Adam

AU - Lüth, Stefan

AU - Buchholz, Frank

AU - Schulze zur Wiesch, Julian

AU - Hauber, Joachim

PY - 2015/9/3

Y1 - 2015/9/3

N2 - Current antiviral therapies cannot cure hepatitis B virus (HBV) infection; successful HBV eradication would require inactivation of the viral genome, which primarily persists in host cells as episomal covalently closed circular DNA (cccDNA) and, to a lesser extent, as chromosomally integrated sequences. However, novel designer enzymes, such as the CRISPR/Cas9 RNA-guided nuclease system, provide technologies for developing advanced therapy strategies that could directly attack the HBV genome. For therapeutic application in humans, such designer nucleases should recognize various HBV genotypes and cause minimal off-target effects. Here, we identified cross-genotype conserved HBV sequences in the S and X region of the HBV genome that were targeted for specific and effective cleavage by a Cas9 nickase. This approach disrupted not only episomal cccDNA and chromosomally integrated HBV target sites in reporter cell lines, but also HBV replication in chronically and de novo infected hepatoma cell lines. Our data demonstrate the feasibility of using the CRISPR/Cas9 nickase system for novel therapy strategies aiming to cure HBV infection.

AB - Current antiviral therapies cannot cure hepatitis B virus (HBV) infection; successful HBV eradication would require inactivation of the viral genome, which primarily persists in host cells as episomal covalently closed circular DNA (cccDNA) and, to a lesser extent, as chromosomally integrated sequences. However, novel designer enzymes, such as the CRISPR/Cas9 RNA-guided nuclease system, provide technologies for developing advanced therapy strategies that could directly attack the HBV genome. For therapeutic application in humans, such designer nucleases should recognize various HBV genotypes and cause minimal off-target effects. Here, we identified cross-genotype conserved HBV sequences in the S and X region of the HBV genome that were targeted for specific and effective cleavage by a Cas9 nickase. This approach disrupted not only episomal cccDNA and chromosomally integrated HBV target sites in reporter cell lines, but also HBV replication in chronically and de novo infected hepatoma cell lines. Our data demonstrate the feasibility of using the CRISPR/Cas9 nickase system for novel therapy strategies aiming to cure HBV infection.

U2 - 10.1038/srep13734

DO - 10.1038/srep13734

M3 - SCORING: Journal article

C2 - 26334116

VL - 5

SP - 13734

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

ER -