Date Published: June 21, 2011
Publisher: Public Library of Science
Author(s): Steven Riley, Kin O. Kwok, Kendra M. Wu, Danny Y. Ning, Benjamin J. Cowling, Joseph T. Wu, Lai-Ming Ho, Thomas Tsang, Su-Vui Lo, Daniel K. W. Chu, Edward S. K. Ma, J. S. Malik Peiris, Lone Simonsen
Abstract: Steven Riley and colleagues analyze a community cohort study from the 2009 (H1N1) influenza pandemic in Hong Kong, and found that more children than adults were infected with H1N1, but children were less likely to progress to severe disease than adults.
Partial Text: Influenza A infection causes substantial morbidity and mortality each year . Periodically, novel human strains emerge, spread rapidly, and cause increased incidence of infection, as was the case with the novel 2009 strain of H1N1 pandemic influenza (H1N1pdm) . However, because many influenza infections are either asymptomatic or cause only mild symptoms, it is difficult to measure infection, rather than clinical disease, across a population . With only clinical data, establishing robust rates of severe disease per infection is difficult. Also, it is not possible to establish traditional risk factors for infection. Hence, it is challenging to generate evidence-based advice for individuals and policy makers about the value of interventions designed to reduce the chance of infection, such as vaccination, social distancing, and other nonpharmaceutical interventions.
The main wave of the 2009 (H1N1) pandemic infected many more children than it did adults. These differences are not explained by baseline antibody titres to H1N1pdm, but could be explained partly by social mixing patterns of the population in these different age strata. However, given that social mixing patterns within the 20–60-y age range do not exhibit substantial variation , and that we have controlled for the presence of a child in the household, it is plausible that increasing age leads to decreased susceptibility independently of mixing and titres to H1N1pdm, possibly as a result of repeated seasonal influenza infections, but by a mechanism not detectable by assays for neutralizing antibody. Whether this reflects antibody that protects by mechanisms other than neutralization, such as antibody-dependent cell cytotoxicity or cell-mediated immunity, remains worthy of investigation.