Autopsy series of 68 cases dying before and during the 1918 influenza pandemic peak.
Identifieur interne : 000E89 ( PubMed/Corpus ); précédent : 000E88; suivant : 000E90Autopsy series of 68 cases dying before and during the 1918 influenza pandemic peak.
Auteurs : Zong-Mei Sheng ; Daniel S. Chertow ; Xavier Ambroggio ; Sherman Mccall ; Ronald M. Przygodzki ; Robert E. Cunningham ; Olga A. Maximova ; John C. Kash ; David M. Morens ; Jeffery K. TaubenbergerSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2011.
English descriptors
- KwdEn :
- MESH :
- chemical , analysis : Antigens, Viral, RNA, Viral.
- epidemiology : Influenza, Human.
- genetics : Influenza A virus.
- history : Influenza, Human.
- immunology : Influenza A virus.
- mortality : Influenza, Human.
- Autopsy, History, 20th Century, Humans, Molecular Sequence Data.
Abstract
The 1918 to 1919 "Spanish" influenza pandemic virus killed up to 50 million people. We report here clinical, pathological, bacteriological, and virological findings in 68 fatal American influenza/pneumonia military patients dying between May and October of 1918, a period that includes ~4 mo before the 1918 pandemic was recognized, and 2 mo (September-October 1918) during which it appeared and peaked. The lung tissues of 37 of these cases were positive for influenza viral antigens or viral RNA, including four from the prepandemic period (May-August). The prepandemic and pandemic peak cases were indistinguishable clinically and pathologically. All 68 cases had histological evidence of bacterial pneumonia, and 94% showed abundant bacteria on Gram stain. Sequence analysis of the viral hemagglutinin receptor-binding domain performed on RNA from 13 cases suggested a trend from a more "avian-like" viral receptor specificity with G222 in prepandemic cases to a more "human-like" specificity associated with D222 in pandemic peak cases. Viral antigen distribution in the respiratory tree, however, was not apparently different between prepandemic and pandemic peak cases, or between infections with viruses bearing different receptor-binding polymorphisms. The 1918 pandemic virus was circulating for at least 4 mo in the United States before it was recognized epidemiologically in September 1918. The causes of the unusually high mortality in the 1918 pandemic were not explained by the pathological and virological parameters examined. These findings have important implications for understanding the origins and evolution of pandemic influenza viruses.
DOI: 10.1073/pnas.1111179108
PubMed: 21930918
Links to Exploration step
pubmed:21930918Le document en format XML
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Kash</name></author><author><name sortKey="Morens, David M" sort="Morens, David M" uniqKey="Morens D" first="David M" last="Morens">David M. Morens</name></author><author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K" last="Taubenberger">Jeffery K. Taubenberger</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigens, Viral (analysis)</term><term>Autopsy</term><term>History, 20th Century</term><term>Humans</term><term>Influenza A virus (genetics)</term><term>Influenza A virus (immunology)</term><term>Influenza, Human (epidemiology)</term><term>Influenza, Human (history)</term><term>Influenza, Human (mortality)</term><term>Molecular Sequence Data</term><term>RNA, Viral (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antigens, Viral</term><term>RNA, Viral</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="history" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autopsy</term><term>History, 20th Century</term><term>Humans</term><term>Molecular Sequence Data</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The 1918 to 1919 "Spanish" influenza pandemic virus killed up to 50 million people. We report here clinical, pathological, bacteriological, and virological findings in 68 fatal American influenza/pneumonia military patients dying between May and October of 1918, a period that includes ~4 mo before the 1918 pandemic was recognized, and 2 mo (September-October 1918) during which it appeared and peaked. The lung tissues of 37 of these cases were positive for influenza viral antigens or viral RNA, including four from the prepandemic period (May-August). The prepandemic and pandemic peak cases were indistinguishable clinically and pathologically. All 68 cases had histological evidence of bacterial pneumonia, and 94% showed abundant bacteria on Gram stain. Sequence analysis of the viral hemagglutinin receptor-binding domain performed on RNA from 13 cases suggested a trend from a more "avian-like" viral receptor specificity with G222 in prepandemic cases to a more "human-like" specificity associated with D222 in pandemic peak cases. Viral antigen distribution in the respiratory tree, however, was not apparently different between prepandemic and pandemic peak cases, or between infections with viruses bearing different receptor-binding polymorphisms. The 1918 pandemic virus was circulating for at least 4 mo in the United States before it was recognized epidemiologically in September 1918. The causes of the unusually high mortality in the 1918 pandemic were not explained by the pathological and virological parameters examined. These findings have important implications for understanding the origins and evolution of pandemic influenza viruses.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21930918</PMID><DateCompleted><Year>2011</Year><Month>11</Month><Day>21</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>108</Volume><Issue>39</Issue><PubDate><Year>2011</Year><Month>Sep</Month><Day>27</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. 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All 68 cases had histological evidence of bacterial pneumonia, and 94% showed abundant bacteria on Gram stain. Sequence analysis of the viral hemagglutinin receptor-binding domain performed on RNA from 13 cases suggested a trend from a more "avian-like" viral receptor specificity with G222 in prepandemic cases to a more "human-like" specificity associated with D222 in pandemic peak cases. Viral antigen distribution in the respiratory tree, however, was not apparently different between prepandemic and pandemic peak cases, or between infections with viruses bearing different receptor-binding polymorphisms. The 1918 pandemic virus was circulating for at least 4 mo in the United States before it was recognized epidemiologically in September 1918. The causes of the unusually high mortality in the 1918 pandemic were not explained by the pathological and virological parameters examined. 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