Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?

This essay proposes that the ecologic association shown between the 20th century coronary heart disease epidemic and the 1918 influenza pandemic could shed light on the mechanism associated with the high lethality of the latter. It suggests that an autoimmune interference at the apoB-LDL interface could explain both hypercholesterolemia and inflammation (through interference with the cellular metabolism of arachidonic acid). Autoimmune inflammation, then, would explain the 1950s-60s acute coronary events (coronary thrombosis upon influenza re-infection) and the respiratory failure seen among young adults in 1918. This hypothesis also argues that the lethality of the 1918 pandemic may have not depended so much on the 1918 virus as on an immune vulnerability to it, possibly resulting from an earlier priming of cohorts born around 1890 by the 1890 influenza pandemic virus.

Saved in:
Bibliographic Details
Main Author: Azambuja,M.I
Format: Digital revista
Language:English
Published: Associação Brasileira de Divulgação Científica 2008
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2008000100001
Tags: Add Tag
No Tags, Be the first to tag this record!
id oai:scielo:S0100-879X2008000100001
record_format ojs
spelling oai:scielo:S0100-879X20080001000012008-06-23Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?Azambuja,M.I Respiratory distress syndrome Autoimmunity Influenza Coronary disease Disease susceptibility Disease outbreaks This essay proposes that the ecologic association shown between the 20th century coronary heart disease epidemic and the 1918 influenza pandemic could shed light on the mechanism associated with the high lethality of the latter. It suggests that an autoimmune interference at the apoB-LDL interface could explain both hypercholesterolemia and inflammation (through interference with the cellular metabolism of arachidonic acid). Autoimmune inflammation, then, would explain the 1950s-60s acute coronary events (coronary thrombosis upon influenza re-infection) and the respiratory failure seen among young adults in 1918. This hypothesis also argues that the lethality of the 1918 pandemic may have not depended so much on the 1918 virus as on an immune vulnerability to it, possibly resulting from an earlier priming of cohorts born around 1890 by the 1890 influenza pandemic virus.info:eu-repo/semantics/openAccessAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research v.41 n.1 20082008-01-01info:eu-repo/semantics/othertext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2008000100001en10.1590/S0100-879X2006005000192
institution SCIELO
collection OJS
country Brasil
countrycode BR
component Revista
access En linea
databasecode rev-scielo-br
tag revista
region America del Sur
libraryname SciELO
language English
format Digital
author Azambuja,M.I
spellingShingle Azambuja,M.I
Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
author_facet Azambuja,M.I
author_sort Azambuja,M.I
title Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
title_short Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
title_full Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
title_fullStr Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
title_full_unstemmed Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
title_sort connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?
description This essay proposes that the ecologic association shown between the 20th century coronary heart disease epidemic and the 1918 influenza pandemic could shed light on the mechanism associated with the high lethality of the latter. It suggests that an autoimmune interference at the apoB-LDL interface could explain both hypercholesterolemia and inflammation (through interference with the cellular metabolism of arachidonic acid). Autoimmune inflammation, then, would explain the 1950s-60s acute coronary events (coronary thrombosis upon influenza re-infection) and the respiratory failure seen among young adults in 1918. This hypothesis also argues that the lethality of the 1918 pandemic may have not depended so much on the 1918 virus as on an immune vulnerability to it, possibly resulting from an earlier priming of cohorts born around 1890 by the 1890 influenza pandemic virus.
publisher Associação Brasileira de Divulgação Científica
publishDate 2008
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2008000100001
work_keys_str_mv AT azambujami connectionscanthe20thcenturycoronaryheartdiseaseepidemicrevealsomethingaboutthe1918influenzalethality
_version_ 1756391209763340288