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By National Research Council (U. S.)

Deals document of the Workshop on improvement of a Polio Antiviral and its power function in international Poliomyelitis Eradication, held November 1-2, 2005. themes comprise public health and wellbeing concerns, power organic goals of polio antiviral medicines, improvement of antiviral medicinal drugs for poliovirus, implementation, and extra. For researchers. Softcover.

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Extra resources for Exploring the Role of Antiviral Drugs in the Eradication of Polio: Workshop Report

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Historically, efforts have focused on the development of antiviral therapeutics to treat rhinovirus infections, such as the common cold. Those efforts led to the elegant studies of structure-based activity of capsid-binding inhibitors, of which pleconaril is the best known example. Pleconaril was evaluated through Phase 3 clinical trials for treatment of the common cold. It had a modest degree of efficacy in the treatment of rhinoviral disease, but licensure by the Food and Drug Administration (FDA), as recommended by an advisory committee, was denied because of the induction of hepatic cytochrome enzymes that altered the metabolism of birth control pills and resulted in intramenstrual bleeding.

Nevertheless, because of the wealth of data gathered over the last 20 years, small molecules with the propensity for occupying the hydrophobic canyon pocket are strong candidates for the development of an antipoliovirus drug. A number of candidates identified during the development of pleconaril may have more activity against poliovirus than against rhinoviruses. Indeed, several potential candidates currently under investigation by ViroDefense, Inc. are further discussed in Chapter 4. B. Drugs Directed Against Non-Structural Proteins It is reasonable to choose proteins encoded in the non-structural region of the genome as targets for anti-poliovirus drugs.

Poliovirus, the prototype of the enteroviruses, has a single-stranded genome (about 7,500 nucleotides) of plus strand polarity (that is, it serves as mRNA in the infected cell) whose nucleotide sequence has been known since 1981 (Kitamura et al. 1981; Racaniello and Baltimore 1981). The genome is protected by a rigid protein shell consisting of multiples of 4 polypeptides. There is no lipid envelope (Rossmann 2002). On entry into a host cell, which is facilitated by the cellular receptor CD155 (also known as Pvr) (Koike et al.

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