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    Equid herpesvirus 1 (EHV1) infection of equine mesenchymal stem cells induces a pUL56-dependent downregulation of select cell surface markers (2015)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Claessen, Christophe
    Favoreel, Herman
    Ma, Guanggang (WE 5)
    Osterrieder, Nikolaus (WE 5)
    De Schauwer, Catharina
    Piepers, Sofie
    Van de Walle, Gerlinde R
    Quelle
    Veterinary Microbiology; 176(1-2) — S. 32–39
    ISSN: 0378-1135
    Sprache
    Englisch
    Verweise
    DOI: 10.1016/j.vetmic.2014.12.013
    Pubmed: 25582614
    Kontakt
    Institut für Virologie

    Robert-von-Ostertag-Str. 7-13
    Gebäude 35
    14163 Berlin
    +49 30 838 51833
    viro@zedat.fu-berlin.de

    Abstract / Zusammenfassung

    Equid herpesvirus 1 (EHV1) is an ubiquitous alphaherpesvirus that can cause respiratory disease, abortion and central nervous disorders. EHV1 is known to infect a variety of different cell types in vitro, but its tropism for cultured primary equine mesenchymal stem cells (MSC) has never been explored. We report that equine MSC were highly permissive for EHV1 and supported lytic replication of the virus in vitro. Interestingly, we observed that an infection of MSC with EHV1 resulted in a consistent downregulation of cell surface molecules CD29 (β1-integrin), CD105 (endoglin), major histocompatibility complex type I (MHCI) and a variable downregulation of CD172a. In contrast, expression of CD44 and CD90 remained unchanged upon wild type infection. In addition, we found that this selective EHV1-mediated downregulation of cell surface proteins was dependent on the viral protein UL56 (pUL56). So far, pUL56-dependent downregulation during EHV1 infection of equine cells has only been described for MHCI, but our present data indicate that pUL56 may have a broader function in downregulating cell surface proteins. Taken together, our results are the first to show that equine MSC are susceptible for EHV1 and that pUL56 induces downregulation of several cell surface molecules on infected cells. These findings provide a basis for future studies to evaluate the mechanisms underlying for this selective pUL56-induced downregulation and to evaluate the potential role of MSC during EHV1 pathogenesis.