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    J Gen Virol. 2010 Sep;91(Pt 9):2152-7. Epub 2010 May 12.

    Herpes simplex virus type 1 entry into epithelial MDCKII cells: role of VASP activities.

    Jaeger V, Hoppe S, Petermann P, Liebig T, Jansen MK, Renné T, Knebel-Mörsdorf D.

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    Max-Planck-Institute for Neurological Research, D-50931 Cologne, Germany.

    Abstract

    VASP is an actin-regulatory protein that links signalling to remodelling of the cytoskeleton. We investigated the role of VASP during entry of herpes simplex viruses into epithelial MDCKII cells. As VASP functions are regulated by phosphorylations, the phosphorylation pattern was determined upon infection. Phosphorylated VASP decreased temporarily at 15 and 30 min after infection. The impact of phosphorylated VASP was addressed by overexpression of phosphomimetic VASP mutants. Our results revealed that phosphorylated VASP slightly reduced the number of infected cells. Expression studies with deletion mutants further indicated minor effects of VASP on infection efficiency, whereas RNA interference studies demonstrated that reduced VASP expression did not suppress infection. We conclude that VASP activities alone may contribute to herpes simplex virus infection to only a minor extent.

    PMID:
    20463151
    [PubMed - indexed for MEDLINE]
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