Host defence mechanisms against influenza infection. II. Protection of mice with vaccines against A/Port Chalmers/1/73 and B/Hong Kong/5/72.

Influenza virus strains A2/Port Chalmers/1/73 (H3N2) and B/Hong Kong/5/72 were adapted to mice by serial passage of virus infected mouse lungs. The adapted viruses were used to challenge mice after they had been immunized with serial dilutions of several bivalent vaccines, containingboth A/Port ChalmersandB/Hong Kong antigens. Vaccines included both whole virus and split-product preparations disrupted by Tween 80 and ether (ET) or tri-N-butyl phosphate (TBP). These bivalent vaccines induced antibodies and conferred protection to mice against challenge with approximately 30 LD50 of the adapted A2/Port Chalmers virus. Significant protection against lethality (P< 0O1) was observed in groups of mice which developed haemagglutinin-inhibition antibody titres of > 1: 16 following immunization. Protection was not statistically significant in groups of mice which developed antibody titres of < 1 : 8 to the A/Port Chalmers/1/73 virus following immunization with higher dilutions of certain vaccines. In a similar fashion, current bivalent vaccines containing B/Hong Kong/5/72 stimulated antibodies and conferred significant protection to immunized mice against lethal challenge with the adapted B/Hong Kong virus. Protection was demonstrated against approximately 30 LD50 of adapted virus in groups of mice which developed mean antibodies of > 1 : 16. Groups of mice, which developed antibody titres of < 1: 8 following immunization with certain dilutions of these vaccines, were not significantly protected. These studies confirm and extend observations made with formerly circulating influenza viruses, i.e. immunization with a specific inactivated vaccine in adequate