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The possibility of system skin reactions caused by amantadine in patients sensitized for tromantadine is discussed. The practical question arises how to handle patients allergic tromantadine patients which may be helped by therapy with amantadine.
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The amantadine derivative 1.3-dimethyl-5-aminoadamantane, D 145, induces in high concentrations of 2-10 mM the release reaction. Adenine nucleotides and 5-hydroxytryptamine (5-HT) are liberated to the same extent and in the same ratio as found after thrombin-induced release. The time course of release is very slow; maximal release is reached in 15-20 min. The process is temperature-dependent and dependent on energy derived from glycolysis and oxidative phosphorylation. Extracellular Ca++ does not promote the release process. D 145, in accordance with the mother-substance amantadine, inhibits 5-HT uptake non-competitively, KI = 0.15mM. In concentrations of 0.1-1 mM D 145 triggers only the liberation of 5-HT, adenine nucleotides are not liberated. The ADP induced platelet aggregation is completely inhibited after preincubation with a 1 mM solution of D 145.
33 different adamntyl amidines containing four different structural types were synthesized and checked for virostatic activity. The activity of compounds of type II seems to originate in their ability to form H-bonds. The strength of antiviral activity is at least partly determined by the electronic effects of substituents at the benzene ring.
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Chronic influenza infection was produced by inoculation with influenza A virus, Waybridge strain (Hav1N1), of continuous murine leukemia Rauscher cells transformed by 20-methylcholantrene. The complete duration of the proliferative-destructive cycle of Rauscher/MX culture infected with fowl plague virus was 24 days on the average. The virus was found in the culture fluid virtually in all stages of the cycle, its titre reaching 10(7) EID50/ml at the peak of the destructive stage. By 14-15 days of the cycle in the chronically infected cells active synthesis of all virus-specific polypeptides (P1, P2, P3, HA, NP, M. NS) was observed, their electrophoretic mobility corresponding completely to that of proteins of the original influenza A virus strain. Simultaneously, almost complete inhibition of synthesis of cellular proteins is observed. Treatment of cultures with amantadine (12.5 micrograms/ml for 4 days) and remantadine (6.25 micrograms/ml for 7 days) interrupted the development of the infectious cycle for 2 1/2-3 1/2 months; during this time cellular protein synthesis recovered and no virus-specific polypeptides were formed. Then, the proliferative-destructive cycle reestablished in the infected cultures.
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The methods of synthesis and antiviral evaluation of 2-(1-adamantyl)imidazole (2a), N-methyl-2-(1-adamantyl)imidazole (2b) and 2-(1-adamantyl)benzimidazole (3a) are reported. These compounds are prepared by the selective homolytic substitution reaction by the adamantyl radical (Ad.) on the C-2 carbon atom of the heterocycles. Ad. radicals were generated by oxidative decarboxylation of 1-adamantyl carboxylic acid. Antiviral activities compounds 2a, 2b and 3a were tested in chick embryos against A-2 Victoria virus. Compounds 2a and 2b showed significant antiviral activity, whereas compound 3a was found inactive.
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The influence of remantadine, ribovirine, and combination thereof on Sindbis virus reproduction in cell cultures was studied. Comparison of remantadine and ribovirine showed the former to be a stronger inhibitor of Sindbis virus reproduction. The results of the combined effect of both drugs in chick embryo fibroblast cultures showed undoubtful advantages of this treatment over the use of each of the drugs alone. In studies of the effect of ribovirine on synthesis of virus-specific proteins and RNA no inhibition of formation of virus-specific macromolecules was observed.
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The effect of one of the derivatives of boraadamantane, preparation BG-12, on reproduction of influenza type A and B viruses was studied. This preparation was shown to inhibit multiplication of a wide range of influenza type A and B virus strains. It is important that BG-12 inhibits in cell culture the replication of a mutant of fowl plague virus A/FPV/Weibridge resistant to remantadine. BG-12 was found to exert a marked viricidal effect, to inhibit the hemolytic activity of both influenza A and influenza B viruses, but not the neuraminidase activity of these viruses. The synthesis of some virus-specific proteins was found to be disturbed in influenza B/Ann Arbor/86-infected cells in the presence of BG-12. A FPVBAR mutant of influenza A/FPV/Weibridge (H7N7) virus resistant to BG-12 was obtained. All the BG-12-resistant reassortants inherited genes 4 and 7 coding for hemagglutinin (HA) and membrane proteins (M) from FPVBAR mutant, respectively, and the remaining genes from BG-12-sensitive A/Krasnodar/101/59 (H2N2) virus. The sequencing of a region of the M gene encoding for the transmembrane protein M2 revealed the substitution of Ala30-Thre in this protein. Multiple attempts at generating a mutant of influenza type B virus resistant to BG-12 failed.
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