Aurora kinase A promotes hepatitis B virus replication and expression

Gi Uk Jeong; Byung Yoon Ahn

doi:10.1016/j.antiviral.2019.104572

Aurora kinase A promotes hepatitis B virus replication and expression

Gi Uk Jeong, Byung Yoon Ahn

Department of Life Sciences

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

Cellular protein kinases play critical roles in various steps of the hepatitis B virus life cycle. We found that viral replication in infected or transfected hepatoma cell was markedly inhibited by treatment with A-443654, a specific inhibitor of Akt. The antiviral mechanism of the drug mainly depended on the downregulation of Aurora A, a protein kinase that plays an essential role in mitosis but has not been implicated in the viral life cycle. Our data indicated that Aurora kinase A enhances viral replication and expression independently of its kinase activity required for mitotic function. Our findings suggest that mitotic kinases, considered to be an attractive target of antitumor agents, also provide a novel target for the development of antiviral therapy.

Original language	English
Article number	104572
Journal	Antiviral Research
Volume	170
DOIs	https://doi.org/10.1016/j.antiviral.2019.104572
Publication status	Published - 2019 Oct

Bibliographical note

Funding Information:
This work was supported by the Basic Science Research Program (# 2018050379 ) of the National Research Foundation of the Ministry of Education of the Republic of Korea . A pilot study was supported by Korea University . G. U. Jeong was supported by the BK21 Plus program.

Publisher Copyright:
© 2019 Elsevier B.V.

Keywords

A-443654
Akt
Antiviral
Aurora kinase
Hepatitis B virus

ASJC Scopus subject areas

Pharmacology
Virology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.antiviral.2019.104572

Cite this

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title = "Aurora kinase A promotes hepatitis B virus replication and expression",

abstract = "Cellular protein kinases play critical roles in various steps of the hepatitis B virus life cycle. We found that viral replication in infected or transfected hepatoma cell was markedly inhibited by treatment with A-443654, a specific inhibitor of Akt. The antiviral mechanism of the drug mainly depended on the downregulation of Aurora A, a protein kinase that plays an essential role in mitosis but has not been implicated in the viral life cycle. Our data indicated that Aurora kinase A enhances viral replication and expression independently of its kinase activity required for mitotic function. Our findings suggest that mitotic kinases, considered to be an attractive target of antitumor agents, also provide a novel target for the development of antiviral therapy.",

keywords = "A-443654, Akt, Antiviral, Aurora kinase, Hepatitis B virus",

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note = "Funding Information: This work was supported by the Basic Science Research Program (# 2018050379 ) of the National Research Foundation of the Ministry of Education of the Republic of Korea . A pilot study was supported by Korea University . G. U. Jeong was supported by the BK21 Plus program. Publisher Copyright: {\textcopyright} 2019 Elsevier B.V.",

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AU - Ahn, Byung Yoon

N1 - Funding Information: This work was supported by the Basic Science Research Program (# 2018050379 ) of the National Research Foundation of the Ministry of Education of the Republic of Korea . A pilot study was supported by Korea University . G. U. Jeong was supported by the BK21 Plus program. Publisher Copyright: © 2019 Elsevier B.V.

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N2 - Cellular protein kinases play critical roles in various steps of the hepatitis B virus life cycle. We found that viral replication in infected or transfected hepatoma cell was markedly inhibited by treatment with A-443654, a specific inhibitor of Akt. The antiviral mechanism of the drug mainly depended on the downregulation of Aurora A, a protein kinase that plays an essential role in mitosis but has not been implicated in the viral life cycle. Our data indicated that Aurora kinase A enhances viral replication and expression independently of its kinase activity required for mitotic function. Our findings suggest that mitotic kinases, considered to be an attractive target of antitumor agents, also provide a novel target for the development of antiviral therapy.

AB - Cellular protein kinases play critical roles in various steps of the hepatitis B virus life cycle. We found that viral replication in infected or transfected hepatoma cell was markedly inhibited by treatment with A-443654, a specific inhibitor of Akt. The antiviral mechanism of the drug mainly depended on the downregulation of Aurora A, a protein kinase that plays an essential role in mitosis but has not been implicated in the viral life cycle. Our data indicated that Aurora kinase A enhances viral replication and expression independently of its kinase activity required for mitotic function. Our findings suggest that mitotic kinases, considered to be an attractive target of antitumor agents, also provide a novel target for the development of antiviral therapy.

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Aurora kinase A promotes hepatitis B virus replication and expression

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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