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    Equid herpesvirus type 4 uses a restricted set of equine major histocompatibility complex class I proteins as entry receptors (2014)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Azab, Walid (WE 5)
    Harman, Rebecca
    Miller, Donald
    Tallmadge, Rebecca
    Frampton, Arthur R
    Antczak, Douglas F
    Osterrieder, Nikolaus (WE 5)
    Quelle
    The journal of general virology; 95(Pt 7) — S. 1554–1563
    ISSN: 0022-1317
    Sprache
    Englisch
    Verweise
    DOI: 10.1099/vir.0.066407-0
    Pubmed: 24722677
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    Institut für Virologie

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    Gebäude 35
    14163 Berlin
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    email:viro@zedat.fu-berlin.de

    Abstract / Zusammenfassung

    Equid herpesvirus type 1 (EHV-1) was shown to use an unusual receptor for cellular entry - MHC-I molecules. Here, we demonstrated that the closely related EHV, EHV-4, also uses this strategy for cellular invasion, both in equine cells in culture and in the heterologous, non-permissive murine mastocytoma cell line (P815) after stable transfection with horse MHC-I genes. Using a panel of P815 cell lines transfected with individual horse MHC-I genes, we provided support for the hypothesis that EHV-1 and EHV-4 target classical polymorphic MHC-I molecules as viral entry receptors. All known equine MHC-I molecules from the two principal classical polymorphic loci specify alanine at position 173 (A173), whilst other MHC-I loci encoded different amino acids at this position and did not permit viral entry. Site-directed mutagenesis of position 173 diminished or enhanced viral entry, depending upon the initial amino acid. However, there were other, as yet undefined, constraints to this process: MHC-I genes from two non-classical loci carried A173 but did not enable viral entry in P815 transfectants. Our study suggested that the capacity to bind MHC-I molecules arose in the common ancestor of EHV-1 and EHV-4. The widespread occurrence of A173 in classical polymorphic horse MHC-I molecules indicated that horses of most MHC haplotypes should be susceptible to infection via this entry portal.