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    Residue 752 in DNA polymerase of equine herpesvirus type 1 is non-essential for virus growth in vitro (2010)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Ma, Guanggang
    Lu, Chengping
    Osterrieder, Nikolaus
    Quelle
    The journal of general virology
    Bandzählung: 91
    Heftzählung: 7
    Seiten: 1817 – 1822
    ISSN: 0022-1317
    Sprache
    Englisch
    Verweise
    DOI: 10.1099/vir.0.018036-0
    Pubmed: 20200193
    Kontakt
    Institut für Virologie

    Robert-von-Ostertag-Str. 7-13
    14163 Berlin
    +49 30 838 51833
    virologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    A single amino acid variation in the equine herpesvirus type 1 (EHV-1) DNA polymerase (Pol) (D752/N752) determines its neuropathogenic potential. Here, an EHV-1 strain RacL11 mutant with a deletion of Pol residue 752 was constructed. The deletion virus was then repaired to encode D752 or N752, respectively. The Delta752 mutant virus replicated with kinetics indistinguishable from those of D752 and N752 viruses. In addition, we could demonstrate that the deletion mutant was significantly more resistant to aphidicolin, a drug targeting Pol, compared with the N752 but not the D752 variant. In equine peripheral blood mononuclear cells, no significant difference was detected between the mutants with respect to cellular tropism or virus replication. The results demonstrated that amino acid residue 752 in EHV-1 Pol is not required for virus growth, and that only the N752 mutation confers a drug-sensitive phenotype to the virus.