Prevention and treatment of lethal influenza A virus bronchopneumonia in mice by monoclonal antibody against haemagglutinin stem region.

The protective properties of monoclonal antibody (MoAb) C179 directed to the stem region of haemagglutinin (HA) H2 that possessed fusion-inhibition and unique broad cross-neutralizing activities were examined in a mouse model. The MoAb efficiently protected mice against a lethal challenge with pneumovirulent human (H1) and avian (H2) strains of influenza A virus. Survival rates in mice that received intraperitonealy (i.

Cross-protection of mice immunized with different influenza A (H2) strains and challenged with viruses of the same HA subtype.

Cross-protection of mice immunized with inactivated preparations of human and avian influenza A (H2) viruses was determined after lethal infection with mouse-adapted (MA) variants of human A/Jap x Bell/57 (H2N1) and avian A/NJers/78 (H2N3) viruses. The MA variants differed from the original strains by acquired virulence for mice and changes in the HA antigenicity. These studies indicated that mice vaccinated with human influenza A (H2) viruses were satisfactorily protected against challenge with A/Jap x Bell/57-MA variant; the survival rate was in the range of 61%-88.

Differences between original strains and their mouse-adapted variants of human (H1) and avian (H2) influenza A viruses in the reaction with cross-neutralizing monoclonal antibody recognizing conformational epitope.

Human (H1) and avian (H2) influenza A viruses and their mouse-adapted (MA) variants were studied in radioimmunoprecipitation assay (RIPA) and infectivity neutralization test using a monoclonal antibody (MoAb) directed against a conserved antigenic epitope in the stem region of the haemagglutinin (HA) and reacting both with H1 and H2 subtypes of HA. Whereas the MA variant of avian influenza A virus differed from the original strain in RIPA and neutralization tests, no differences were observed between the original human strain and its MA variant, as well as between the original H1 and H2 strains.

Changes of morphological, biological and antigenic properties of avian influenza A virus haemagglutinin H2 in the course of adaptation to new host.

The alterations of avian influenza A virus haemagglutinin (HA) H2 as a result of adaptation to mice were first investigated in this study. HA of mouse-adapted (MA) variant was somewhat different from that of the original strain in electrophoretical mobility, antigenic structure and in haemagglutination activity with mouse red blood cells.

Principles of selective inactivation of viral genome. VIII. The influence of beta-propiolactone on immunogenic and protective activities of influenza virus.

The influence of beta-propiolactone action on the immunogenic and protective activity of the influenza virus A/WSN/33 (H1N1) has been studied. The production of antibodies against virion surface antigens in mice immunized intramuscularly by the modified virus was enhanced with the increase of inoculating dose from 6 x 10(7) to 1.5 x 10(8) viral particles per animal.

Effects of UV-irradiation upon Venezuelan equine encephalomyelitis virus.

Venezuelan equine encephalomyelitis virus labelled with [14C]aminoacids or [3H]uridine was purified and UV-irradiated. The irradiation led to the formation of uracil photodimers and the covalent linking of the nucleocapsid protein C to virion RNA. The inactivation of infectivity correlated with the formation of uracil dimers, whereas the RNA-protein links were formed at much higher doses of UV irradiation.

The genetic aspects of influenza virus filamentous particle formation.

We analysed the genetic content of reassortants between parent viruses differing in their ability to form filaments. The results suggest that primarily HA, M, and NP genes are involved in the control of the filament forming ability. A lower buoyant density of the filamentous forms as compared to spherical particles allowed us to obtain a sufficiently pure population of filaments.