Role of simvastatin and methyl-beta-cyclodextrin [corrected] on inhibition of poliovirus infection.

Cells exposed to simvastatin or to methyl-beta-cyclodextrin show reduced poliovirus infection, without alteration in virus binding or on the kinetics of genome entry, suggesting that the steps which are altered are those post uncoating and genome entry. Reduction of infection by cyclodextrin is reversed by increasing MOI whereas that produced by simvastatin treatment is not, suggesting that the effects on infection are not due to a reduction in cholesterol. The differences in the characteristics of inhibition can be explained by the differential effects of the compounds.

Poliovirus binding to its receptor in lipid bilayers results in particle-specific, temperature-sensitive channels.

Poliovirus (PV) infection starts with binding to its receptor (PVR), followed by a receptor-aided, temperature-sensitive conformational change of the infectious particle (sedimenting at 160S) to a particle which sediments at 135S. Reported in this communication is the successful incorporation into lipid bilayers of two forms of the receptor: the full-length human receptor and a modified clone in which the extracellular domains of the receptor were fused to a glycosylphosphatidylinositol tail. Addition of virus (160S) to receptor-containing bilayers leads to channel formation, whereas no channels were observed when the receptor-modified viral particle (135S) was added.

Microfabricated teflon membranes for low-noise recordings of ion channels in planar lipid bilayers.

We present a straightforward, accessible method for the fabrication of micropores with diameters from 2 to 800 micro m in films of amorphous Teflon (Teflon AF). Pores with diameters View Article and Find Full Text PDF