a point mutation in a herpesvirus polymerase determines neuropathogenicity点突变在疱疹病毒聚合酶决定neuropathogenicity.pdfVIP
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a point mutation in a herpesvirus polymerase determines neuropathogenicity点突变在疱疹病毒聚合酶决定neuropathogenicity
A Point Mutation in a Herpesvirus Polymerase
Determines Neuropathogenicity
1 2 3 4 5 2
Laura B. Goodman , Arianna Loregian , Gillian A. Perkins , Josie Nugent , Elizabeth L. Buckles , Beatrice Mercorelli ,
4¤a ` 2 4¤b 1* 4¤c
Julia H. Kydd , Giorgio Palu , Ken C. Smith , Nikolaus Osterrieder , Nicholas Davis-Poynter
1 Department of Microbiology and Immunology, Cornell University, Ithaca, New York, United States of America, 2 Department of Histology, Microbiology and Medical
Biotechnologies, University of Padua, Padua, Italy, 3 Department of Clinical Sciences, Cornell University, Ithaca, New York, United States of America, 4 Centre for Preventive
Medicine, Animal Health Trust, Newmarket, United Kingdom, 5 Department of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America
Infection with equid herpesvirus type 1 (EHV-1) leads to respiratory disease, abortion, and neurologic disorders in
horses. Molecular epidemiology studies have demonstrated that a single nucleotide polymorphism resulting in an
amino acid variation of the EHV-1 DNA polymerase (N752/D752) is significantly associated with the neuropathogenic
potential of naturally occurring strains. To test the hypothesis that this single amino acid exchange by itself influences
neuropathogenicity, we generated recombinant viruses with differing polymerase sequences. Here we show that the
N752 mutant virus caused no neurologic signs in the natural host, while the D752 virus was able to cause inflammation
of the central nervous system and ataxia. Neurologic disease induced by the D752 virus was
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