Abstract
BackgroundDuring the 2009 influenza pandemic, individuals over the age of 60 had the lowest incidence of infection with approximately 25% of these people having pre-existing, cross-reactive antibodies to novel 2009 H1N1 influenza isolates. It was proposed that older people had pre-existing antibodies induced by previous 1918-like virus infection(s) that cross-reacted to novel H1N1 strains.Methodology/Principal FindingsUsing antisera collected from a cohort of individuals collected before the second wave of novel H1N1 infections, only a minority of individuals with 1918 influenza specific antibodies also demonstrated hemagglutination-inhibition activity against the novel H1N1 influenza. In this study, we examined human antisera collected from individuals that ranged between the ages of 1 month and 90 years to determine the profile of seropositive influenza immunity to viruses representing H1N1 antigenic eras over the past 100 years. Even though HAI titers to novel 2009 H1N1 and the 1918 H1N1 influenza viruses were positively associated, the association was far from perfect, particularly for the older and younger age groups.Conclusions/SignificanceTherefore, there may be a complex set of immune responses that are retained in people infected with seasonal H1N1 that can contribute to the reduced rates of H1N1 influenza infection in older populations.
Highlights
The influenza antigens hemagglutinin (HA) and neuraminidase (NA) are the major surface glycoproteins of the virus and immune protective targets
As previously described [9], hemagglutination-inhibition assay (HAI) titers ($1:40 HAI titer as positive) were determined for 1918 and novel H1N1 viruses for each serum sample collected from a cohort of people representing ages 1 month to 90 years of age for the novel H1N1 isolate A/California/ 7/2009 [9] or A/Mexico/4108/2009 (Fig. 1)
The novel 2009 H1N1 influenza virus emerged in March, 2009 and rapidly spread around the world resulting in the first influenza pandemic of the 21st century
Summary
The influenza antigens hemagglutinin (HA) and neuraminidase (NA) are the major surface glycoproteins of the virus and immune protective targets. Changes (antigenic drift and shift) in these HA and NA proteins can result in evasion of pre-existing neutralizing antibodies within a host. Antigenic shifts led to 3 influenza pandemics over the last century resulting in significant morbidity and mortality. Human H1N1 serotypes persisted as seasonal influenza until 1957, when they were replaced by the H2N2 virus [4]. In 1968, the H2N2 isolates were replaced in the human population by viruses of the H3N2 subtype. During the 2009 influenza pandemic, individuals over the age of 60 had the lowest incidence of infection with approximately 25% of these people having pre-existing, cross-reactive antibodies to novel 2009 H1N1 influenza isolates. It was proposed that older people had pre-existing antibodies induced by previous 1918-like virus infection(s) that crossreacted to novel H1N1 strains
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