The therapeutic activity of arbidol was investigated against representatives of seven different virus families. Its 50% median effective concentration (EC(50) ) was 0.22-11.8 µg/ml (0.41-22 nM). Therapeutic indices of 91 were obtained for type 1 poliovirus and 1.9-8.5 for influenza A and B, human paramyxo-3, avian infectious bronchitis-, and Marek's disease viruses. Arbidol was more inhibitory for influenza A/Aichi/2/68 (H3N2) virus than rimantadine or amantadine (EC(50) 10 vs. >15 and >31.6 µg/ml); greater inhibition occurred when end-points were expressed as TCID(50) s. For respiratory syncytial virus (RSV), a reduction in plaque size but not number was observed. However, when the drug was added to infected cultures (≥5 µg/ml), a 3-log reduction in titer occurred. Arbidol did not inhibit directly influenza A/Aichi/2/68 hemagglutinin (HA) or neuraminidase (NA) activity, but inhibition of fusion between the viral envelope and chicken red blood cells occurred when added at 0.1 µg/ml prior to infection. Arbidol induced changes to viral mRNA synthesis of the PB2, PA, NP, NA, and NS genes in MDCK cultures infected with influenza A/PR/8/34. There was no indirect evidence of enhancement of interferon-α by arbidol following infection with A/Aichi/2/68. Arbidol neither reduced lung viral titers nor caused a significant reduction of lung consolidation in BALB/c mice after administration by the oral and intraperitoneal (i.p.) routes and intranasal challenge with influenza A/Aichi/2/68. A small reduction in lung consolidation, but not viral titer, occurred after i.p. administration and subsequent challenge with RSV. The results indicate the potential of arbidol as a broad-spectrum respiratory antiviral drug.

Children aged 7-14 years in Novgorod, Russia, were given Russian live cold-adapted or inactivated influenza vaccines or placebo over a 2-year period. Schools were randomly assigned as a whole to one of the preparations. In the first year, the vaccines were bivalent, containing types A (H3N2) and A (H1N1) components. In the second year, the vaccines also contained a type B component. In the first year, all viruses isolated were type A (H3N2); in the second, about three-quarters of the isolates were type B and the rest type A (H1N1). During both years, the vaccines protected the vaccinated children. Where significant differences existed, the live attenuated vaccine was more protective than the inactivated. Vaccination rates in schools in which live attenuated vaccines had been used were inversely related to illness rates of staff and unvaccinated children, suggesting that viral transmission had been reduced by the vaccine.

SUMMARYThe specificity of serum anti-HA antibody from children immunized or infected with A/Victoria/75 (H3N2) or A/Texas/77 (H3N2) virus was examined using the single radial haemolysis test together with adsorption of antibody with three antigenic variants A/Hong Kong/68 (H3N2), A/Port Chalmers/73 (H3N2) and A/Victoria/75 (H3N2). The majority of young children reacted to vaccination or infection by producing strain-specific (SS) antibody to the homologous virus. A small proportion of children's sera contained cross-reacting (CR) antibodies capable of reacting with the haemagglutinins of all antigenic variants of the subtype including A/HK/1/68. In contrast, most adults reacted immunologically to either vaccination or infection by producing CR antibody, reacting with all variants of the antigenic subtype including the prototype virus A/HK/1/68 (H3N2).

Thirty-seven volunteers were inoculated intranasally with living attenuated influenza A2 viruses. Rising titres of circulating antineuraminidase (AN) were detected in 14 of 17 infected volunteers. AN was also found in nasal secretions. Statistical analysis showed that there was a correlation between the titres of haemagglutination-inhibiting antibody (HI) and AN in nasal washings, and between AN in blood and washings. Resistance to infection could be predicted from antibody titres in 29 of 37 volunteers and blood AN alone predicted the outcome of 25 volunteers.