Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite

Shinn Jong Jiang; Tsun Mei Lin; Guey Yueh Shi; Hock Liew Eng; Hsiao Yen Chen; Hua Lin Wu

doi:10.1016/j.antiviral.2004.04.003

Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite

Shinn Jong Jiang, Tsun Mei Lin, Guey Yueh Shi, Hock Liew Eng, Hsiao Yen Chen, Hua Lin Wu^*

^*Corresponding author for this work

Graduate Institute of Clinical Medical Sciences

National Cheng Kung University

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

1 Scopus citations

Abstract

The effect of arsenite pretreatment on bovine herpesvirus-4 (BHV-4) replication in bovine arterial endothelial (BAE) cells was studied. BHV-4 infectivity, including IE-2 expression, DNA replication and viral yield, were significantly reduced at nontoxic concentrations of arsenite in which cellular DNA synthesis or cell viability of BAE cells were not affected under resting and confluent conditions. This effect was accompanied by the induction of heat shock protein 70 (HSP70) and an interrupted cell cycle (causing cell cultures to accumulate at the S and G2/M phases). Actinomycin D inhibited the induction of HSP70 and reduced arsenite antiviral activity. In conclusion, cellular stress response induced by arsenite in BAE cells inhibited replication of BHV-4, and probably resulted from the induction of HSP70 and interference of cell cycle progression.

Original language	English
Pages (from-to)	167-175
Number of pages	9
Journal	Antiviral Research
Volume	63
Issue number	3
DOIs	https://doi.org/10.1016/j.antiviral.2004.04.003
State	Published - 09 2004

Keywords

Arsenite
Bovine herpesvirus-4
Endothelial cells
HSP70

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10.1016/j.antiviral.2004.04.003

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title = "Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite",

abstract = "The effect of arsenite pretreatment on bovine herpesvirus-4 (BHV-4) replication in bovine arterial endothelial (BAE) cells was studied. BHV-4 infectivity, including IE-2 expression, DNA replication and viral yield, were significantly reduced at nontoxic concentrations of arsenite in which cellular DNA synthesis or cell viability of BAE cells were not affected under resting and confluent conditions. This effect was accompanied by the induction of heat shock protein 70 (HSP70) and an interrupted cell cycle (causing cell cultures to accumulate at the S and G2/M phases). Actinomycin D inhibited the induction of HSP70 and reduced arsenite antiviral activity. In conclusion, cellular stress response induced by arsenite in BAE cells inhibited replication of BHV-4, and probably resulted from the induction of HSP70 and interference of cell cycle progression.",

keywords = "Arsenite, Bovine herpesvirus-4, Endothelial cells, HSP70",

author = "Jiang, {Shinn Jong} and Lin, {Tsun Mei} and Shi, {Guey Yueh} and Eng, {Hock Liew} and Chen, {Hsiao Yen} and Wu, {Hua Lin}",

year = "2004",

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doi = "10.1016/j.antiviral.2004.04.003",

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journal = "Antiviral Research",

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T1 - Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite

AU - Jiang, Shinn Jong

AU - Lin, Tsun Mei

AU - Shi, Guey Yueh

AU - Eng, Hock Liew

AU - Chen, Hsiao Yen

AU - Wu, Hua Lin

PY - 2004/9

Y1 - 2004/9

N2 - The effect of arsenite pretreatment on bovine herpesvirus-4 (BHV-4) replication in bovine arterial endothelial (BAE) cells was studied. BHV-4 infectivity, including IE-2 expression, DNA replication and viral yield, were significantly reduced at nontoxic concentrations of arsenite in which cellular DNA synthesis or cell viability of BAE cells were not affected under resting and confluent conditions. This effect was accompanied by the induction of heat shock protein 70 (HSP70) and an interrupted cell cycle (causing cell cultures to accumulate at the S and G2/M phases). Actinomycin D inhibited the induction of HSP70 and reduced arsenite antiviral activity. In conclusion, cellular stress response induced by arsenite in BAE cells inhibited replication of BHV-4, and probably resulted from the induction of HSP70 and interference of cell cycle progression.

AB - The effect of arsenite pretreatment on bovine herpesvirus-4 (BHV-4) replication in bovine arterial endothelial (BAE) cells was studied. BHV-4 infectivity, including IE-2 expression, DNA replication and viral yield, were significantly reduced at nontoxic concentrations of arsenite in which cellular DNA synthesis or cell viability of BAE cells were not affected under resting and confluent conditions. This effect was accompanied by the induction of heat shock protein 70 (HSP70) and an interrupted cell cycle (causing cell cultures to accumulate at the S and G2/M phases). Actinomycin D inhibited the induction of HSP70 and reduced arsenite antiviral activity. In conclusion, cellular stress response induced by arsenite in BAE cells inhibited replication of BHV-4, and probably resulted from the induction of HSP70 and interference of cell cycle progression.

KW - Arsenite

KW - Bovine herpesvirus-4

KW - Endothelial cells

KW - HSP70

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Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite

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