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Arbidol research index:

Voprosy Virusologii Mar-Apr;51(2):20-2 2006 English (professional translation .pdf)

The efficacy of antiviral preparations in vitro on the reproduction of influenza virus strains A/H5N1, which caused an epizootic among domesticated birds in summer 2005

D. K. Lvov, I. T. Fedyakina, M. Yu. Shchelkanov, A. G. Prilipov, P. G. Deryabin, G. A. Galegov

The commercial drugs rimantadine, amantadine, ribavirin and arbidol are effective in suppressing in in vitro reproduction of highly pathogenic avian influenza A/H5N1 viruses. This study was done on porcine embryo kidney (SPEV) cells and the highly pathogenic A/Duck/Novosibirsk/ 56/05(H5N1) strain from an infected domestic duck (anas platyrhynchos domesticus) in the Lake Chany area, Novosibirsk region.

Original Russian Document .pdf

Ter Arkh. 2005;77(8):84-8. English (professional translation .html)

Sensitivity of various influenza virus strains to arbidol. Influence of arbidol combination with different antiviral drugs on reproduction of influenza virus A

Leneva IA, Fediakina IT, Gus'kova TA, Glushkov RG.

AIM: To study antiviral activity of arbidol in relation to various antigenic subtypes of influenza virus isolated from humans; efficacy of arbidol action in combination with adamantanic antiviral drugs, ribavirin and ribamidil on reproduction of influenza virus A (IVA) in cell culture. MATERIAL AND METHODS: The activity of the drugs against viral reproduction was assessed by inhibition of viral antigens expression detected in virus-infected cells using enzyme immunoassay (EIA). RESULTS: Arbidol is just as good as adamantanic drugs, neuraminidase inhibitors, ribavirin and ribamidil by its inhibiting activity in relation to influenza viruses A and B. Arbidol inhibits reproduction of human IVA antigenic strains H1N1, H2N2, H3N2 and remantadin-sensitive and remantadin-resistant strains of influenza virus. Arbidol inhibits reproduction of pathogenic for humans strains of avian influenza virus H5N1 and H9N2, strains H6N1 and H9N2 having internal genes common with H5N1 and H9N2. The inhibiting activity of arbidolin on cell culture viral reproduction enhanced if arbidol was used in combination with amantadine, remantadin, ribavirin and ribamidil. CONCLUSION: Arbidol has a wide spectrum antiviral activity and inhibits reproduction of various antigenic subtypes and remantadin-resistent human IVA, avian viruses H5N1 and H9N2, influenza viruses B and C.

PMID: 16206613 [PubMed - indexed for MEDLINE]

Original Russian Document .pdf

Vopr Virusol. 2005 Nov-Dec;50(6):32-5 English (professional translation .html)

Sensitivity of influenza A/H5 viruses isolated from wild birds on the territory of Russia to arbidol in the cultured MDCK cells

The effect of the antiviral drug arbidol on the reproduction of avian influenza A/H5 viruses was studied in in vitro experiments. The strains were isolated from the wild birds of Eastern Siberia and they were closely related to the 1997-2000 viruses from South-Eastern Asia. Arbidol was shown to exert a selective inhibiting effect on the reproduction of these viruses in the MDCH cell cultures.

PMID: 16408629 [PubMed - in process]

Original Russian Document .pdf

Emerging Infectious Diseases EID-05-1609 Research 12-Dec-2005 English publication .pdf

Characterization of highly pathogenic avian influenza (HPAI) A subtype H5N1 strains isolated from an outbreak in poultry and wild birds in Western Siberia, July 2005

Lvov, Dmitry; D.I. Ivanovsky Institute of Virology, Virus ecology Prilipov, Alex; D.I. Ivanovsky Institute of Virology, Molecular genetics, et al

Arbidol hydrochloride Coxsackievirus group B3 Antiviral effect

Abstract: Complete genomes of two highly pathogenic avian influenza (HPAI) A (H5N1) strains isolated from wild birds (A/Grebe/Novosibirsk/29/05) and poultry (A/Duck/Novosibirsk/56/05) during an epizootic in 2005 summer in one location in Western Siberia (Novosibirsk region, Russia) were analyzed. These strains had a basic amino acid motif in the hemagglutinin cleavage site characteristic of HPAI influenza. They differed genetically from the H5N1 avian viruses isolated earlier but were closely related in all genes to the H5N1 viruses isolated from wild birds in Qinghai Lake, China, in May 2005. There was slight genetic differences between the two Western Siberian strains (2005) within the PB1, PB2, PA and NP genes (from one to four amino acid substitutions), but both viruses had Lys-627 in PB2 protein, Glu-92 in NS1, Ser-31 in M2 and a 20-mer deletion in the NA gene. Both isolates were sensitive to remantadine, amantadine, ribavirin, arbidol in porcine embryo kidney cell line.

ANTIVIRAL RESEARCH 65 (3): A63-A64 MAR 2005 - Full text not available at this time

The Features of Antiviral Action of Arbidol—Selection and Characterization of Arbidol-resistant Mutants

Irina A. Leneva1, Alexander M. Shuster2, Alan J. Hay3, Robert G. Glushkov1
1Department of Chemotherapy of Infectious Diseases, Center of Chemistry of Drugs-Russian Chemical and Pharmaceutical Institute, Moscow, Russia; 2‘Masterlek’, Moscow, Russia; 3National Institute for Medical Research, London, UK

An antiviral drug arbidol (1-metyl-2-phenyl-thiomethyl
6-bromoindolehydrochloride monohydrate) is widely used for prophylaxis and therapy of influenza A and B in Russia. The study of effect of arbidol on viral replication showed that arbidol inhibited viral reproduction of all antigen subtype of human influenza A and B viruses, avian influenza viruses, possessing H5 and H9, and rimantadine-resistant strains of influenza A viruses. Arbidol demonstrated broad-spectrum antiviral activity against respiratory viruses inhibiting RSV and adenovirus type 3 viral replication in cell culture.

Arbidol was previously shown to inhibit early stage of influenza A virus replication. The studies of the arbidol effect upon replication of panel of reassortants between A/Singapore/1/57(H2N2) and A/Chiken/Germany/27 (Weybridge strain, H7N7) showed that the greater sensitivity of the Weybridge virus to arbidol was determined by the HA gene; there was no correlation between sensitivity to arbidol and any other gene Arbidol-resistant mutants were obtained by passing viruses in MDCK cells in the presence of increasing drug concentrations. Mutants selected for resistance to arbidol promoted membrane fusion at higher pH (0.2–0.4) than wild-type virus. Arbidol inhibited haemolysis induced by the wild-type virus, but did not inhibit the haemolysis induced by arbidol-resistant mutants. To determine the molecular basic of the arbidol-resistance the HA genes of the wild-type and arbidol-resistant mutants were sequenced.

All mutants had amino acid substitutions only in HA2 subunit, but at different positions. The study of the effect of arbidol on conformation of the HA using conformational antibodies showed that arbidol caused conformational change in the structure of HA of wild-type virus, but not in arbidol-resistant mutants. The data indicate that the target of arbidol is the HA and that arbidol increases its stability to low pH-induced changes and as a consequence inhibits membrane fusion during virus infection.

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