Purified influenza A virus N2 neuraminidase vaccine is immunogenic and non-toxic in humans.

The immunogenicity and toxicity of a purified influenza virus (N2) neuraminidase vaccine (NAV) were investigated in 88 human subjects aged 18-40, and compared to response to a conventional trivalent influenza vaccine, Fluogen (Parke-Davis). NAV doses ranged from 2.6 to 69.

Preparation and characterization of a purified influenza virus neuraminidase vaccine.

Influenza virus neuraminidase (NA) has been shown to induce protective but infection-permissive immunity in experimental animals. Challenge infection following such immunization is attended by decreased viral replication and disease manifestations but is sufficient to provide antigenic stimulation and definitive immunity to the virus. The present report describes the preparation and characterization of a purified NA vaccine (NAV) used in Phase 1 (immunogenicity and toxicity) trials in humans.

Infection-permissive immunization with influenza virus neuraminidase prevents weight loss in infected mice.

In studies of infection of young Balb/c mice with a mouse virulent strain of X-31 (H3N2) influenza A virus we have shown a profound virus dose-related effect of infection on body weight. Most of this effect is prevented by prior administration of either inactivated whole virus vaccine, which prevents infection, or purified influenza virus neuraminidase, which is infection-permissive, but reduces pulmonary virus replication by 1.5 to 3 orders of magnitude.

Independent and disparate evolution in nature of influenza A virus hemagglutinin and neuraminidase glycoproteins.

The hemagglutinin (HA) and neuraminidase (NA) external glycoprotein antigens of H1N1 and H3N2 subtypes of epidemiologically important influenza A viruses prevalent during recent decades were subjected to intensive antigenic analysis by four different methods. Prior to serological analysis with polyclonal rabbit antisera, HA and NA antigens of four viruses of each subtype were segregated by genetic reassortment to forestall nonspecific steric hindrance during antigen-antibody combination. This analysis has demonstrated that with respect to antigenic phenotype, HA and NA proteins have evolved at different rates.