By Y. Becker (auth.), Yechiel Becker, Julia Hadar (eds.)
ISBN-10: 1461338042
ISBN-13: 9781461338048
ISBN-10: 1461338069
ISBN-13: 9781461338062
Research on antiviral medicinal drugs and their mode of motion in contaminated cells. in animals and in guy. has ended in a greater realizing of the molecular professional cesses all in favour of virus replication. Screeninq of enormous numbers of common and semisynthetic compounds ended in the characterization of sure sub stances that had a constrained potency as antiviral druqs. a number of chemically synthesized compounds have been additionally chanced on to be potent as antiviral brokers within the chemotherapy of human virus illnesses. a big trouble within the enhance ment of potent antiviral brokers has been the inability of selectivity. and toxicity for uninfected cells. of gear that successfully inhibited virus replication in vitro. additional knowing of the molecular techniques of virus replication in contaminated cells has led to the advance of recent antivirals directed at virus-coded enzymes or proteins. contemporary reviews on antivirals which are activated through the herpes simplex virus style l-coded thy midine kinase from a prod rug to an antiviral drug have opened new instructions within the improvement of powerful antiviral medications. the current booklet bargains with a couple of antiviral medicines potent opposed to herpes simplex viruses and offers a few perception into the molecular elements of virus replication. It additionally throws mild at the new techniques to the advance of antiviral medications. The molecular foundation of the antiviral job of recent and recognized medications and their attainable use in chemotherapy of viral sickness are offered during this book.
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Extra info for Antiviral Drugs and Interferon: The Molecular Basis of Their Activity
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28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. , Strickland, S. C. Ann. Y. Acad. Sci. C. H. Invest. Opthalmol. li:470-478, 1976. C. H. Proc. Soc. Exp. BioI. Med. ~:9296, 1977. S. H. J. Infect. Diseases lil:575-579, 1980. , Stebbing, N. H. , ~:393-404, 1981. S. H. A:3491-3494, 1980. T. H. J. Gen. Virol. ~:481-492, 1974. S. H. J. BioI. Chern. 1979. -S. -C. -C. Biochim. Biophys. Acta ~:370-381, 1976. Ostrander, M. -C. Biochim. Biophys. Acta ~:232-235, 1980. , Goz, B. H. Biochim. Biophys. Acta ~:253-263, 1975.
If derivatives of EHNA with greater anti- viral potency can be obtained they may be useful antiviral drugs, particularly if they fail to inhibit ADA. Several lines of evidence suggest that the inhibition of HSV by EHNA is not due solely to inhibition of ADA. ADA is 2-4 x 10 ~ First of all, the K. of EHNA for inhibition of 1 M (26) whereas inhibition of HSV replication by 50% requires 4-8 x 10-6M (Figure '4). Secondly, the more potent inhibitor of ADA, DCF, does not inhibit replication of HSV (Figure 4).
Treatment of HSV-infected cells with EHNA leads to decreases in levels of all four dNTPs, measured at 6 hr post-infection. These concentrations of EHNA have much less effect on dNTP pools in uninfected cells 47 that are treated with EHNA in the same manner. Levels of dNTPs have been reported to increase after infection of cells with HSV (37). Results in Table I show that this is particularly true for dTTP and dGTP, which increase in concentration several-fold after infection. 5-fold. crease somewhat after infection.
Antiviral Drugs and Interferon: The Molecular Basis of Their Activity by Y. Becker (auth.), Yechiel Becker, Julia Hadar (eds.)
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