Titlebook: Antiviral Drug Development; A Multidisciplinary Erik Clercq,Richard T. Walker Conference proceedings 1988 Plenum Press, New York 1988 anti

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GRAVE

Robert C. Morrison,Robert G. Parrflected in a measurable difference in sensitivity between the mutant and parental strain. Such resistance has now been observed in widely divergent virus families to a variety of specific inhibitors; some important examples are summarised in Table 1.

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ANA

Electronic Density Functional Theoryof the organism, absent in cell culture, are required to convert the drug into its effective form. Most of the time, however, the reverse is true, viz. more compounds do appear active in a cell culture system than will later be found useful in the organism (Buthala, 1965; Eggers, 1977b). I shall refer to this problem in a later section.

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Rachel Y. W. Lau,Hilary J. Kahnn equine encephalomyelitis virus on the other hand (4). Especially the latter indicates that a non-immune mechanism was responsible. Although the most simple explanation for tissue immunity is a direct interaction between the different viruses, it has been assumed for a long time that a non-viral agent was responsible for this effect (3,5).

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Molecular Targets for Selective Antiviral Chemotherapy,f herpetic encephalitis), ribavirin for the topical (aerosol) treatment of respiratory syncytial virus infection in infants, and retrovir (azidothymidine) for the systemic (intravenous or peroral) treatment of AIDS and AIDS-related complex (ARC)..

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Enzyme