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J Gen Virol. 2010 Dec;91(Pt 12):3002-9. doi: 10.1099/vir.0.024166-0. Epub 2010 Sep 1.

Phosphoinositide 3 kinase signalling may affect multiple steps during herpes simplex virus type-1 entry.

Author information

1
Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, IL 60612, USA.

Abstract

Early interactions of herpes simplex virus type-1 (HSV-1) with cells lead to cytoskeletal changes facilitating filopodia formation and membrane fusion. Here, we demonstrate that phosphoinositide 3 kinase (PI3K) signalling may affect multiple steps during HSV-1 entry. An inhibitor of PI3K (LY294002) blocked HSV-1 entry and the blockage was cell-type- and gD receptor-independent. Entry inhibition was also observed with primary cultures of the human corneal fibroblasts and unrelated β- and γ-herpesviruses. Immunofluorescence analysis demonstrated that LY294002 negatively affected HSV-1-induced filopodia formation. Similar effects of the inhibitor were seen on HSV-1 glycoprotein-induced cell-to-cell fusion. Cells expressing HSV-1 glycoproteins (gB, gD, gH and gL) showed significantly less fusion with target cells in the presence of the inhibitor. Expression of a dominant-negative PI3K mutant negatively affected both entry and fusion. We also show that inhibition of PI3K signalling also affected RhoA activation required for HSV-1 entry into certain cell types.

PMID:
20810749
PMCID:
PMC3052565
DOI:
10.1099/vir.0.024166-0
[Indexed for MEDLINE]
Free PMC Article

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