A2 Antibody Research Articles

Antineuraminidase Antibody Response of Man to Influenza Virus Neuraminidase N2: Results Obtained with an Improved Hemagglutination Inhibition Technique and an Enzyme Inhibition Test

Abstract Sets of sera obtained from subjects vaccinated or infected with influenza A2 strains from 1957 to 1968 were examined by an improved hemagglutination inhibition procedure for measuring antineuraminidase antibodies with recombinant viruses, and by a neuraminidase inhibition test with human serum Cohn fraction IV-4 as substrate. Recombinants prepared with viruses containing 1957 and 1968 antigenic variants of neuraminidase were employed. The improved HI procedure was found to be as reliable as the NI test for detecting antineuraminidase antibody and antineuraminidase antibody increase. Antineuraminidase antibody was generally not found on first exposure to A2 strains but antibody increase occurred with increasing frequency during subsequent years. The antineuraminidase antibody response of man is broad, making recognition of antigenic enzymatic variants difficult by use of human serum.

Postnatal decline of maternally acquired viral antibodies of different specificities

The rates of decline (half-lives) of maternally acquired antibodies of two different specificities in a group of infants were found to be highly variable, ranging from 18 to 192 days for parainfluenza type 3 antibody (54 infants) and from 15 to 251 days for influenza A2 antibody (nine infants). For antibodies of both specificities approximately 75% of the half-lives were between 15 and 60 days. With parainfluenza type 3 antibody, and possibly with influenza A2 antibody, the half-lives were inversely proportional to the initial antibody titre of the babies' sera. This relationship could be described by a rectangular hyperbola. Babies with high antibody titres at birth lost this antibody rapidly whereas in babies with low initial titres antibody declined over a longer period.The half-lives of parainfluenza type 3 antibody and influenza A2 antibody were compared with that of rubella antibody in the same group of infants (previously published). Maternally acquired viral antibodies of different specificities did not necessarily decline at similar rates in any given child. In nine infants, maternally acquired antibodies of two different specificities (rubella and parainfluenza type 3) declined at significantly different rates in the same child. It is suggested that although the half-life of antibody of a given specificity is related to its concentration in the serum, it is independent of the level of serum antibodies of other specificities.

Preparation and Properties of Antibody Directed Specifically Against the Neuraminidase of Influenza Virus

Summary Antiserum was prepared against a recombinant influenza virus possessing A0 (NWS strain) type hemagglutinin and A2 (RI/5+) type neuraminidase. This antiserum was absorbed sequentially with NWS and A2 viruses and antibody directed against A2 type neuraminidase was then dissociated from the A2 virus. This antibody had no activity against the hemagglutinin activity of A0, A1 and A2 influenza viruses or against the infectivity of A0 and A1 viruses. It neutralized the enzyme activity of A2 but not A0 or A1 type influenza viruses. Anti-enzyme antibody caused apparent neutralization of the infectivity of influenza viruses possessing A2 type neuraminidase providing that the antibody was allowed to remain in contact with the cells during the test period. This antibody did not prevent infection of susceptible cells but apparently prevented the release of detectable levels of hemagglutinin. It had no effect on the infectivity of an A2 type recombinant virus that lacked neuraminidase activity.

INFLUENZA HAEMAGGLUTINATION-INHIBITION ANTIBODIES IN SYDNEY.

Haemagglutination-inhibiting antibodies against A, A′ and A2strains of influenza virus and against one strain of influenza B were estimated in sera from blood donors in Sydney in February 1958 and in April and October 1961.The A2antibody increased substantially while both A and A′ antibodies declined slightly. There was a great decline in influenza B antibody during the same period.Thanks are due to Dr Phyllis M. Rountree who suggested this study. Miss Patricia Taylor gave excellent technical assistance in the early part of this work.