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A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice.

A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Research Abstract Details 

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  • A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Abstract Text:

    kevin r mottKevin R Mott,guey-chuen perngGuey-Chuen Perng,yanira osorioYanira Osorio,konstantin g kousoulasKonstantin G Kousoulas,homayon ghiasiHomayon Ghiasi,kevin r mottKevin R Mott,guey-chuen perngGuey-Chuen Perng,yanira osorioYanira Osorio,konstantin g kousoulasKonstantin G Kousoulas,homayon ghiasiHomayon Ghiasi,

    The effect of glycoprotein K (gK) overexpression on herpes simplex virus type 1 (HSV-1) infection in two different strains of mice was evaluated using a recombinant HSV-1 virus that expresses two additional copies of the gK gene in place of the latency-associated transcript (LAT). This mutant virus (HSV-gK3) expressed higher levels of gK than either the wild-type McKrae virus or the parental dLAT2903 virus both in vitro (in cultured cells) and in vivo (in infected mouse corneas and trigeminal ganglia [TG] of BALB/c and C57BL/6 mice). gK transcripts were detected in the TG of both HSV-gK3-infected mouse strains on day 30 postinfection (p.i.), while gB transcripts were detected only in the TG of the HSV-gK3-infected C57BL/6 mice, a finding that suggests that increased gK levels promote chronic infection. C57BL/6 mice infected with HSV-gK3 also contained free virus in their TG on day 30 p.i. Both HSV-gK3-infected mouse strains had significantly higher corneal scarring (CS) than did McKrae-infected mice. T-cell depletion studies in C57BL/6 mice suggested that this CS enhancement in the HSV-gK3-infected mice was mediated by a CD8+ T-cell response. Taken together, these results strongly suggest that increased gK levels promote eye disease and chronic infection in infected mice.

    A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Publishing Authors By Initials

    kr mottKR Mott,gc perngGC Perng,y osorioY Osorio,kg kousoulasKG Kousoulas,h ghiasiH Ghiasi,kr mottKR Mott,gc perngGC Perng,y osorioY Osorio,kg kousoulasKG Kousoulas,h ghiasiH Ghiasi,

    For similar biological factors: toxins, biological: virulence factors research abstracts see: biological factors: toxins, biological: virulence factors research

    PUBMED ID PMID:

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    A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Journal Published:

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

    Journal: Journal of virology

    VOLUME: 81

    Page Numbers: 12962-72

    Journal Abbreviation: J. Virol.

    ISSN: 1098-5514

    DAY: 26

    MONTH: 09

    YEAR: 2007

    A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 113724

    A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Keywords Mesh Terms:

    KEYWORDS: Virulence Factors

    MESH TERMS: physiology

    Chemical & Substance for Abstract: A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice. Information

    Substance Name: latency associated transcript protein, h

    Registry Number: 0

    Grant and Affiliation Information for A recombinant herpes simplex virus type 1 expressing two additional copies of gK is more pathogenic than wild-type virus in two different strains of mice.

    AFFILIATION: Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, CSMC-D2024, 8700 Beverly Blvd., Los Angeles, California 90048, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NEI

    GRANT: EY13615

    ACRONYM: EY

    MEDLINETA: J Virol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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