Binding of herpes simplex virus type-1 virions leads to the induction of intracellular signalling in the absence of virus entry.

ABSTRACT: The envelope of HSV-1 contains a number of glycoproteins, four of which are essential for virus entry. Virus particles lacking gB, gD, gH or gL are entry-defective, although these viruses retain the ability to bind to the plasma membrane via the remaining glycoproteins. Soluble forms of gD have been shown to trigger the nuclear translocation of the NF-kappaB transcriptional complex in addition to stimulating the production of Type I interferon. By taking advantage of the entry-defective phenotype of glycoprotein-deficient HSV-1 virus particles, the results presented here show that binding of virions to cellular receptors on the plasma membrane is sufficient to stimulate a change in cellular gene expression. Preliminary microarray studies, validated by quantitative real-time PCR, identified

SUBMITTER: MacLeod IJ 

PROVIDER: S-EPMC2832691 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature