Giuseppe
Emeritus
[Source: Epidemics, via ScienceDirect, full text: (LINK). Abstract, edited.]
Epidemics
Volume 3, Issue 1, March 2011, Pages 46-60 <HR SIZE=1>
doi:10.1016/j.epidem.2011.02.001 | How to Cite or Link Using DOI
Copyright ? 2011 Elsevier B.V. All rights reserved.
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Geography May Explain Adult Mortality from the 1918?20 Influenza Pandemic
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Svenn-Erik Mamelund<SUP>a</SUP><SUP>, </SUP>
<SUP>a</SUP> The Norwegian Institute of Public Health, Division for Infectious disease control, Department of Vaccines, P.O. Box 4404 Nydalen, 0403 Oslo, Norway
Received 12 August 2009; revised 21 January 2011; accepted 3 February 2011. Available online 10 February 2011.
Abstract
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.
Keywords: Immunology; Indigenous populations; Historical epidemiology; Genetic diversity; Environmental factors
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Epidemics
Volume 3, Issue 1, March 2011, Pages 46-60 <HR SIZE=1>
doi:10.1016/j.epidem.2011.02.001 | How to Cite or Link Using DOI
Copyright ? 2011 Elsevier B.V. All rights reserved.
Permissions & Reprints
Geography May Explain Adult Mortality from the 1918?20 Influenza Pandemic
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Svenn-Erik Mamelund<SUP>a</SUP><SUP>, </SUP>
<SUP>a</SUP> The Norwegian Institute of Public Health, Division for Infectious disease control, Department of Vaccines, P.O. Box 4404 Nydalen, 0403 Oslo, Norway
Received 12 August 2009; revised 21 January 2011; accepted 3 February 2011. Available online 10 February 2011.
Abstract
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.
Keywords: Immunology; Indigenous populations; Historical epidemiology; Genetic diversity; Environmental factors