Key result
Rhinovirus IRES function in neuronal cell types depends on specific structural elements within the 3' non-translated region of the viral genome, suggesting long-range interactions.
Long-range interactions between the IRES and the 3' terminus control IRES-mediated gene expression and virus propagation in neuronal cells, explaining the cell type-specific defect of rhinovirus IRES.
Hypothesis-generating for rhinovirus neuronal tropism; leaves open effects on clinical outcomes or cardiovascular complications.
We have proposed a cancer treatment modality based on poliovirus chimeras replicating under the translational control of an internal ribosomal entry site (IRES) derived from human rhinovirus type 2. Insertion of the heterologous IRES causes a neuron-specific propagation deficit and eliminates neurovirulence inherent in poliovirus without affecting viral growth in cells derived from malignant gliomas. We now report the elucidation of a molecular mechanism responsible for the cell type-specific defect mediated by the rhinovirus IRES. Rhinovirus IRES function in neuronal cell types depends on specific structural elements within the 3' non-translated region of the viral genome. Our observations suggest long-range interactions between the IRES and the 3' terminus that control IRES-mediated gene expression and virus propagation.
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Dobrikova et al. (2003) studied Malignant gliomas. Poliovirus chimeras with human rhinovirus type 2 IRES was evaluated on IRES function and virus propagation in neuronal cell types. Rhinovirus IRES function in neuronal cell types depends on specific structural elements within the 3' non-translated region of the viral genome, suggesting long-range interactions.
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