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Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript.

Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Research Abstract Details 

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  • Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Abstract Text:

    ling jinLing Jin,guey-chuen perngGuey-Chuen Perng,dale carpenterDale Carpenter,kevin r mottKevin R Mott,nelson osorioNelson Osorio,julia naitoJulia Naito,david j brickDavid J Brick,clinton jonesClinton Jones,steven l wechslerSteven L Wechsler,

    Latency-associated transcript (LAT) significantly enhances the spontaneous reactivation phenotype of herpes simplex virus type 1 (HSV-1). The mechanism by which LAT accomplishes this has been elusive. To determine if LAT's antiapoptosis activity is involved, the authors used a rabbit eye model to analyze the spontaneous reactivation phenotype of an HSV-1 mutant in which LAT was replaced by an unrelated antiapoptosis gene. This virus, dLAT-cpIAP, contains the open reading frame of the baculovirus inhibitor of apoptosis protein gene (cpIAP) in place of LAT, under control of the LAT promoter. The authors report here that in a rabbit ocular model of infection, dLAT-cpIAP had a spontaneous reactivation phenotype similar to wild-type virus and significantly higher than LAT(-) viruses. This was consistent with their previous findings using the mouse trigeminal ganglia explant-induced reactivation model. Whether LAT (and in the case of dLAT-cpIAP, cpIAP) enhances the spontaneous reactivation phenotype by functioning during establishment of latency, maintenance of latency, or reactivation from latency, or during two or more of these periods, remains to be determined. Regardless, the results presented in this study strongly support the hypothesis that LAT's antiapoptosis activity is the dominant function that enhances HSV-1's spontaneous reactivation phenotype.

    Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Publishing Authors By Initials

    l jinL Jin,gc perngGC Perng,d carpenterD Carpenter,kr mottKR Mott,n osorioN Osorio,j naitoJ Naito,dj brickDJ Brick,c jonesC Jones,sl wechslerSL Wechsler,

    For similar biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: viral physiology: virus replication research abstracts see: biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: viral physiology: virus replication research

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    Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Journal of neurovirology

    VOLUME: 13

    Page Numbers: 78-84

    Journal Abbreviation:

    ISSN: 1355-0284

    DAY: 3

    MONTH: 12

    YEAR: 2007

    Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9508123

    Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Keywords Mesh Terms:

    KEYWORDS: Virus Replication

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript. Information

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    Grant and Affiliation Information for Reactivation phenotype in rabbits of a herpes simplex virus type 1 mutant containing an unrelated antiapoptosis gene in place of latency-associated transcript.

    AFFILIATION: The Eye Institute, University of California Irvine, School of Medicine, Irvine, California 92697, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCRR

    GRANT: P20RR15635

    ACRONYM: RR

    MEDLINETA: J Neurovirol

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