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[The mechanisms of the antiviral action of the bora-adamantane derivative preparation BG-12].

Identifieur interne : 002D77 ( Main/Exploration ); précédent : 002D76; suivant : 002D78

[The mechanisms of the antiviral action of the bora-adamantane derivative preparation BG-12].

Auteurs : S G Markushin ; B V Sinitsyn ; V P Ginzburg ; A M Kha Der ; A I Klimov

Source :

RBID : pubmed:8073750

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English descriptors

Abstract

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.

PubMed: 8073750


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Le document en format XML

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<front>
<div type="abstract" xml:lang="en">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.</div>
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