Seroprevalence following the second wave of Pandemic 2009 H1N1 influenza in Pittsburgh, PA, USA

Abstract

Background: In April 2009, a new pandemic strain of influenza infected thousands of persons in Mexico and the United States and spread rapidly worldwide. During the ensuing summer months, cases ebbed in the Northern Hemisphere while the Southern Hemisphere experienced a typical influenza season dominated by the novel strain. In the fall, a second wave of pandemic H1N1 swept through the United States, peaking in most parts of the country by mid October and returning to baseline levels by early December. The objective was to determine the seroprevalence of antibodies against the pandemic 2009 H1N1 influenza strain by decade of birth among Pittsburgh-area residents.

Methods and findings: Anonymous blood samples were obtained from clinical laboratories and categorized by decade of birth from 1920-2009. Using hemagglutination-inhibition assays, approximately 100 samples per decade (n = 846) were tested from blood samples drawn on hospital and clinic patients in mid-November and early December 2009. Age specific seroprevalences against pandemic H1N1 (A/California/7/2009) were measured and compared to seroprevalences against H1N1 strains that had previously circulated in the population in 2007, 1957, and 1918. (A/Brisbane/59/2007, A/Denver/1/1957, and A/South Carolina/1/1918). Stored serum samples from healthy, young adults from 2008 were used as a control group (n = 100). Seroprevalences against pandemic 2009 H1N1 influenza varied by age group, with children age 10-19 years having the highest seroprevalence (45%), and persons age 70-79 years having the lowest (5%). The baseline seroprevalence among control samples from 18-24 year-olds was 6%. Overall seroprevalence against pandemic H1N1 across all age groups was approximately 21%.

Conclusions: After the peak of the second wave of 2009 H1N1, HAI seroprevalence results suggest that 21% of persons in the Pittsburgh area had become infected and developed immunity. Extrapolating to the entire US population, we estimate that at least 63 million persons became infected in 2009. As was observed among clinical cases, this sero-epidemiological study revealed highest infection rates among school-age children.

Figure 1. Allegheny County, Pennsylvania pandemic H1N1 cases.

Sampling period for serosurvey (November 16-December 4, 2009) shown relative to epidemic curve. Distribution of the novel H1N1 vaccine to health clinics began in late-November.

Figure 2. Percent seropositive (HAI≥1∶40) by decade of birth for A/California/7/2009; H1N1 influenza.

Figure 3. Seropositive samples for historical influenza A H1N1 strains (A/Brisbane/59/2007, Denver/1/1957 and A/South Carolina/1/1918).

Figure 4. Genetic relatedness of HA from historical strains of influenza H1N1.

The tree includes select H1N1 influenza isolates of the classic swine and human influenza lineages (see Materials and Methods for database accession numbers). Phylogenetic trees were inferred from hemagglutinin amino acid sequences using the maximum likelihood method. Bootstrap analysis values are shown above the branches. The scale bar indicates the number of amino acid residue changes per unit length of the horizontal branches.