Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells.

Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Research Abstract Details 

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Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Abstract Text:

Ying-Hsiu Su,Xianchao Zhang,Xiaohe Wang,Nigel W Fraser,Timothy M Block,

Following infection, the physical state of linear herpes simplex virus (HSV) genomes may change into an "endless" or circular form. In this study, using Southern blot analysis of the HSV genome, we provide evidence that immediate-early protein ICP4 is involved in the process of converting the linear HSV-1 ICP4-deleted mutant strain d120 genome into its endless form. Under conditions where de novo viral DNA synthesis was inhibited, the genome of the ICP4 deletion mutant d120 failed to assume an endless conformation following infection of Vero cells (compared with the ability of wild-type strain KOS). This defect was reversed in the Vero-derived cell line E5, which produces the ICP4 protein, suggesting that ICP4 is necessary and sufficient to complement the d120 defect. When ICP4 protein was provided by the replication-defective DNA polymerase mutant HP66, the genomes of mutant d120 could assume an endless conformation in Vero cells. Western blot analysis using antibody specific to the ICP4 protein showed that although the d120 virions contained ICP4 protein, the majority of that ICP4 protein was in a 40-kDa truncated form, with only a small fraction present as a full-length 175-kDa protein. When expression of ICP4 protein from E5 cells was inhibited by cycloheximide, the d120 virion-associated ICP4 protein was unable to mediate endless formation after infection of E5 cells. Collectively, these data suggest that ICP4 protein has an important role in mediating the endless formation of the HSV-1 genome upon infection and that this function can be provided in trans.

Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Publishing Authors By Initials

YH Su,X Zhang,X Wang,NW Fraser,TM Block,

For similar cells: cells, cultured: cell line: vero cells research abstracts see: cells: cells, cultured: cell line: vero cells research

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Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of virology

VOLUME: 80

Page Numbers: 11589-97

Journal Abbreviation: J. Virol.

ISSN: 0022-538X

DAY: 20

MONTH: 09

YEAR: 2006

Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 113724

Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Keywords Mesh Terms:

KEYWORDS: Vero Cells

MESH TERMS: physiology

Chemical & Substance for Abstract: Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells. Information

Substance Name: herpes simplex virus, type 1 protein ICP

Registry Number: 0

Grant and Affiliation Information for Evidence that the immediate-early gene product ICP4 is necessary for the genome of the herpes simplex virus type 1 ICP4 deletion mutant strain d120 to circularize in infected cells.

AFFILIATION: Department of Microbiology and Immunology, Drexel Institute for Biotechnology and Virology Research, College of Medicine, Drexel University, 3805 Old Easton Road, Doylestown, PA 18901-2697, USA. ys98@drexel.edu

Country: United States

AGENCY: United States NINDS

GRANT: NS 33768

ACRONYM: NS

MEDLINETA: J Virol

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