Reichert et al. also attribute this age structure to original antigenic sin but emphasize the importance of exposures to the changing hemagglutinin glycosylation patterns of earlier influenza (H1N1) subtypes (eg, those circulating before and after 1948) on a background of relatively conserved T-cell epitopes (14). However, the possibility that the age structure of pandemic (H1N1) 2009 infection is due simply to single or repeated exposures to different or differentially exposed hemagglutinin epitopes has not been ruled out. Useful information bearing on these questions might be gained by comparing antibody levels, antibody reactivities, and the original antigenic sin phenomenon in serum samples from the various age cohorts that had early exposures to markedly different (or to no) influenza (H1N1) serotypes, eg, persons born before 1918; during 1918–1927, 1928–1946, 1947–1956, and 1957–1976; and after 1976. Of related interest are the 2009 influenza experiences of the≈ 25.6 million persons living in America vaccinated with the 1976 Hsw1N1 vaccine (17), including 2.5 million born during 1957–1975, when influenza (H1N1) viruses did not circulate

The current pandemic provides the challenge to public health responses that Adjala and Henderson describe, as well as an opportunity to extend the efforts of Francis to better understand the complicated epidemiology of influenza. Is original antigenic sin really a sin from which our immune systems need to be saved? Or is it an epidemiologic blessing in disguise? We have much more to learn. As St. Augustine wrote (Confessiones, 8, 7):“Lord make me chaste—but not yet.”