Seasonal influenza takes its most pronounced toll on children and the elderly, giving the crude age-specific mortality rates a U-shape. In contrast, A(H1N1) 1918-20 pandemic mortality was W-shaped. When adjusting for the seasonal baseline, young adults had higher but the elderly lower than expected mortality. The lower than expected mortality for the elderly is one reason why total mortality in urban societies were relatively low in 1918-20 (<1%). Why mortality peaked at age 30 but declined into old age is still not clear. It has been suggested that cohorts >30 years was protected because they were exposed to H1-like viruses prior to 1889. This hypothesis assumes that people lived within the reach of the urban disease pools. Here I analyze mortality after age 30 in aboriginal populations assumed to be infrequently exposed to influenza due to their geographic isolation. Results show that Arctic and Pacific peoples also experienced a decline in relative mortality after age 30. However, the remotely living elderly did not have lower than expected mortality, suggesting that they had less prior exposure to influenza than their urban counterpart. Crude total mortality and mortality for all adults >30 years was nevertheless extremely high in the remote populations. Parish records quantitatively confirmed the anecdotes that children 5-14 years were the only survivors in some Arctic communities. Low exposure to H1-like viruses in adults could not alone explain the high total mortality in remote populations (up to 90%). A high concurrent disease load, crowding, low genetic variability, a lack of basic care, and infrequent exposure to other forms of influenza virus 1890-1917 may have played a role as well. This form of immunological cross-protection from previous exposure to A-type influenza viruses other than H1N1 can only be explained as a consequence of cellular immunity against internal proteins that show less inter-strain variation than the surface proteins.
Copyright © 2011 Elsevier B.V. All rights reserved.