Abstract
An initial stage of infection mechanism of plant virus was explained from physicochemical point of view using model lipid membrane such as monolayer and/or liposome. Thus, the differences of self-assemble processes, secondary structures, penetration modes of plant virus coat proteins such as strong virus (tobacco mosaic virus, TMV) and its mutant, sensitive virus (cucumber green mottle mosaic virus, CGMMV) to lipid membrane were discussed. It was suggested that TMV protein having hydrophobic sites penetrated more to hydrophobic domains of lipid membrane. When we used the lipid membrane including a specific binding substance to TMV extracted from plasma membrane, TMV protein penetrated much more to membrane, but its structural change was small. The antiviral activity of polysaccharides on infectivity of virus was caused by blocking the decapsulation process of virus coat protein which occurs on the cell membrane in the initial stage of virus infection. These results suggest that it is possible to search a new and strong antiviral reagents from the biophysical-chemical view point.
