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AbstractThe effect of the drug Stimforte on infection by the Hepatitis C virus (HCV) has been studied. Stimforte partially inhibits HCV infection at a dose of 100 μg/mouse and almost completely at a dose of 300 μg/mouse within 24 h after administration of the drug. The mice sera resulting after 24 h in the presence of 100 and 300 µg/mouse of Stimforte effectively inhibit the production of HCV. Doses of 150, 200, and 250 µg/mouse are not effective. Stimulation of interferon-β (IFN-β) production is only observed at doses of 100 and 300 µg/mouse, which explains well the neutralizing capacity of the sera. The amount of IFN-γ also correlates well with the antiviral activity and neutralizing activity of mice sera. The drug practically does not stimulate production of IFN-λ. Thus, the neutralizing activity of sera and the antiviral activity are largely determined by the 1st and 2nd IFN groups.

AbstractStimforte in a wide range of concentrations (15–225 µg/mL) totally inhibits the cytopathic activity of hepatitis C virus (HCV) in the Vero-V cell culture. Interferons (IFN) play the most important role in the suppression of infection when the drug is introduced into the culture before the infection. When Stimforte is introduced after the infection, the mechanism of action seems to be different. The activators of IFN production are mainly (or exclusively) the ligands of receptor complexes TLR-4 and NOD-2 contained in the drug. The action of these substances is probably synergistic, similar to the action of LPS and MDP in Vero-V cells.

Fractions of Inonotus obliquus fungus water extract exhibited a virucidal effect towards hepatitis C virus: it 100-fold reduced its infective properties within 10 min. The antiviral effects of fungus extracts manifested after preventive (24 h before infection) and therapeutic use (during infection of porcine embryo kidney cells). Moreover, the data indicate that the birch fungus extracts inhibit production of infective virus by porcine embryo kidney cells.

Fifty-four strains of H5N1 highly pathogenic avian influenza (HPAI) virus were isolated from wild birds in the ecosystems of northern Eurasia and from poultry in the south of western Siberia (July 2005), at the mouth of Volga River (November 2005), at Uvs-Nur Lake on the boundary of the Great Lakes Depression in western Mongolia and the Tyva Republic of Russia (June 2006), in the vicinity of Moscow (February 2007), in the southeastern part of the Russian Plain (September 2007 and December 2007), and in the far east (April 2008) of the Russian Federation and were phenotypically characterized and deposited into the Russian state collection of viruses. Complete genome nucleotide sequences for 24 strains were obtained and deposited into GenBank. In all cases when strains were isolated from both wild birds and poultry in the same outbreak these strains were genetically closely related to each other. Until 2008 all HPAI H5N1 strains isolated in northern Eurasia clustered genetically with the viruses from Kukunor Lake (Qinghai Province, China), known as genotype 2.2 or the “Qinghai-Siberian” genotype. The viruses from the Qinghai-Siberian genotype have continued to evolve from those initially introduced into western Siberia in 2005 into two genetic groups: “Iran–North Caucasian” and “Tyva-Siberian.” In vitro replication potential (50% tissue-culture infectious dose in porcine embryo kidney) of Qinghai-Siberian strains decreased over time, which could reflect decreasing virulence. Comparison of genome sequences with biological characteristics of the respective strains permitted us to identify point mutations in PB2, PB1, PA, HA, NP, NA, M2, NS1, and NS2 that possibly influenced the level of replication potential. The HPAI H5N1 virus, which penetrated into the south of the Russian Far East in spring 2008, belonged to genotype 2.3.2.

Stimforte, an immune response-stimulating preparation, is active with respect to hepatitis C virus (HCV) and herpes simplex virus type I (HSV-1). The effects of Stimforte in animals infected with either HCV or HSV-1 are fundamentally different. In mice with acute herpes virus infection, Stimforte administration leads to a higher activity of natural killer cells and cytotoxic lymphocytes, and the amount of interferon (IFN) λ grows. In mice infected with HCV, Stimforte administration results in a significant increase in IFN-β but not IFN-λ in blood and affected organs. Stimforte has been found to affect directly HCV reproduction that causes the infected cell death, but it does not affect HSV-1 reproduction in the Vero cells (V).

This paper presents the results of experimental study of the combined anti-influenza action of ribavirin and ozeltamivir on the reproduction of several subtypes of influenza viruses A, including those resistant to rimantadine.

Antiviral activity of a Russian drug flakozid towards infection caused by a cytopathogenic variant of hepatitis C virus in SPEV cells is studied. Flakozid is an individual natural flavonoid glycoside 7-O-β-D-glucopyranoside-8-(methyl-but)-2-enyl)-5,4’-dioxyflavanolol), isolated from the leaves of Phellodendron amurense Rupr. and Ph. amurense var. lavallei (Dode) Sprague, Rutaceae family. High antiviral activity of flakozid manifests in response to its addition into the monolayer of SPEV cells infected by hepatitis C virus during all periods of experiment. Flakozid exhibits weak cytotoxicity and no viricidal activity towards hepatitis C virus, which is comparable to activity of ribavirin (antiviral drug). Chemotherapeutic index of flakozid is 15-25 times higher than that of the reference drug ribavirin.

Antiviral properties of Hexoral (0.1% solution and 0.2% aerosol for local application) and its constituent hexetidine against viruses causing human respiratory tract infections and herpes virus were studied in vitro . It was found that non-cytotoxic concentrations of hexetidine (alone and as a component of Hexoral) attenuated infectious properties of highly virulent influenza virus A/H5N1, pandemic influenza virus A/H1N1pdm, respiratory syncytial virus, and herpes simplex virus type 1 after a short-term exposure (30 sec) by 100 or more times. It was found that hexidine mostly contributes to the virucidal effect of Hexoral.

New amino acid derivatives with carbocycles of adamantine and quinaldic acid were synthesized and their in vitro antiviral activity against influenza A/H5N1 virus was evaluated. Experiments on cultured embryonic porcine kidney epithelial cells showed that amino acid derivatives suppressed viral replication. Tret-butyloxycarbonyl-DL-methionylsulfonyl-1-adamantayl ethylamine and benzyloxycarbonyl-L-trypthophanyl-1-adamantayl ethylamine compounds demonstrated high activity in all in vitro experiments. Moreover, some compounds showed virucidal activity against influenza A/H5N1 virus.

We studied the capacity amino acid derivatives of adamantane to inhibit replication of highly virulent avian influenza A/duck/Novosibirsk/56/05 (H5N1) virus in cultures of swine embryonic kidney cells. Amino acid derivatives of adamantane H-His-Rem and Ad(CH 2 -Ser-OMe) 2 were characterized by lower toxicity than remantadine previously used in the treatment of influenza. Histidine-containing adamantane derivative (H-His-Rem) was the most effective and low-toxic inhibitor of influenza А/H5N1 virus replication and can be recommended for clinical trials to produce a preparation for the treatment and prevention of influenza.