Key result
A proposed model for poliovirus cell entry suggests that receptor binding acts as a transition-state catalyst to release the mature virion from a metastable state, initiating pore formation.
The proposed model for poliovirus cell entry shares striking structural and mechanistic parallels with the maturation and cell entry of more complex enveloped viruses like influenza and HIV.
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Hypothesis-generating for picornavirus and enveloped virus entry; leaves open antiviral applications pending experimental validation.
Structural studies of polio- and closely related viruses have provided a series of snapshots along their cell entry pathways. Based on the structures and related kinetic, biochemical, and genetic studies, we have proposed a model for the cell entry pathway for polio- and closely related viruses. In this model a maturation cleavage of a capsid protein precursor locks the virus in a metastable state, and the receptor acts like a transition-state catalyst to overcome an energy barrier and release the mature virion from the metastable state. This initiates a series of conformational changes that allow the virus to attach to membranes, form a pore, and finally release its RNA genome into the cytoplasm. This model has striking parallels with emerging models for the maturation and cell entry of more complex enveloped viruses such as influenza virus and HIV.
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James M. Hogle (2002) conducted a review in Poliovirus infection. A proposed model for poliovirus cell entry suggests that receptor binding acts as a transition-state catalyst to release the mature virion from a metastable state, initiating pore formation.
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