Multinational impact of the 1968 Hong Kong influenza pandemic : Evidence for a smoldering pandemic
Identifieur interne : 000051 ( PascalFrancis/Corpus ); précédent : 000050; suivant : 000052Multinational impact of the 1968 Hong Kong influenza pandemic : Evidence for a smoldering pandemic
Auteurs : Cécile Viboud ; Rebecca F. Grais ; Bernard A. P. Lafont ; Mark A. Miller ; Lone SimonsenSource :
- The Journal of infectious diseases [ 0022-1899 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Background. The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period. Methods. We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank. Results. In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen. Conclusion. We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970.
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| NO : | PASCAL 05-0376425 INIST |
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| ET : | Multinational impact of the 1968 Hong Kong influenza pandemic : Evidence for a smoldering pandemic |
| AU : | VIBOUD (Cécile); GRAIS (Rebecca F.); LAFONT (Bernard A. P.); MILLER (Mark A.); SIMONSEN (Lone) |
| AF : | Fogarty International Center, National Institutes of Health/Bethesda, Maryland/Etats-Unis (1 aut., 2 aut., 4 aut.); National Institute of Allergy and Infectious Diseases, National Institutes of Health/Bethesda, Maryland/Etats-Unis (3 aut., 5 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2005; Vol. 192; No. 2; Pp. 233-248; Bibl. 53 ref. |
| LA : | Anglais |
| EA : | Background. The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period. Methods. We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank. Results. In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen. Conclusion. We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970. |
| CC : | 002A05; 002B05 |
| FD : | Hong Kong; Microbiologie; Infection; Grippe A |
| FG : | Chine; Asie; Virose |
| ED : | Hong Kong; Microbiology; Infection; Influenza A |
| EG : | China; Asia; Viral disease |
| SD : | Hong Kong; Microbiología; Infección; Gripe A |
| LO : | INIST-2052.354000138405420060 |
| ID : | 05-0376425 |
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P." last="Lafont">Bernard A. P. Lafont</name><affiliation><inist:fA14 i1="02"><s1>National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Miller, Mark A" sort="Miller, Mark A" uniqKey="Miller M" first="Mark A." last="Miller">Mark A. Miller</name><affiliation><inist:fA14 i1="01"><s1>Fogarty International Center, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Simonsen, Lone" sort="Simonsen, Lone" uniqKey="Simonsen L" first="Lone" last="Simonsen">Lone Simonsen</name><affiliation><inist:fA14 i1="02"><s1>National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">05-0376425</idno><date when="2005">2005</date><idno type="stanalyst">PASCAL 05-0376425 INIST</idno><idno type="RBID">Pascal:05-0376425</idno><idno type="wicri:Area/PascalFrancis/Corpus">000051</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Multinational impact of the 1968 Hong Kong influenza pandemic : Evidence for a smoldering pandemic</title><author><name sortKey="Viboud, Cecile" sort="Viboud, Cecile" uniqKey="Viboud C" first="Cécile" last="Viboud">Cécile Viboud</name><affiliation><inist:fA14 i1="01"><s1>Fogarty International Center, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Grais, Rebecca F" sort="Grais, Rebecca F" uniqKey="Grais R" first="Rebecca F." last="Grais">Rebecca F. Grais</name><affiliation><inist:fA14 i1="01"><s1>Fogarty International Center, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lafont, Bernard A P" sort="Lafont, Bernard A P" uniqKey="Lafont B" first="Bernard A. P." last="Lafont">Bernard A. P. Lafont</name><affiliation><inist:fA14 i1="02"><s1>National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Miller, Mark A" sort="Miller, Mark A" uniqKey="Miller M" first="Mark A." last="Miller">Mark A. Miller</name><affiliation><inist:fA14 i1="01"><s1>Fogarty International Center, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Simonsen, Lone" sort="Simonsen, Lone" uniqKey="Simonsen L" first="Lone" last="Simonsen">Lone Simonsen</name><affiliation><inist:fA14 i1="02"><s1>National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">The Journal of infectious diseases</title><title level="j" type="abbreviated">J. infect. dis.</title><idno type="ISSN">0022-1899</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">The Journal of infectious diseases</title><title level="j" type="abbreviated">J. infect. dis.</title><idno type="ISSN">0022-1899</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Hong Kong</term><term>Infection</term><term>Influenza A</term><term>Microbiology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Hong Kong</term><term>Microbiologie</term><term>Infection</term><term>Grippe A</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background. The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period. Methods. We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank. Results. In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen. Conclusion. We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-1899</s0></fA01><fA02 i1="01"><s0>JIDIAQ</s0></fA02><fA03 i2="1"><s0>J. infect. dis.</s0></fA03><fA05><s2>192</s2></fA05><fA06><s2>2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Multinational impact of the 1968 Hong Kong influenza pandemic : Evidence for a smoldering pandemic</s1></fA08><fA11 i1="01" i2="1"><s1>VIBOUD (Cécile)</s1></fA11><fA11 i1="02" i2="1"><s1>GRAIS (Rebecca F.)</s1></fA11><fA11 i1="03" i2="1"><s1>LAFONT (Bernard A. P.)</s1></fA11><fA11 i1="04" i2="1"><s1>MILLER (Mark A.)</s1></fA11><fA11 i1="05" i2="1"><s1>SIMONSEN (Lone)</s1></fA11><fA14 i1="01"><s1>Fogarty International Center, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="02"><s1>National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA17 i1="01" i2="1"><s1>Multinational Influenza Seasonal Mortality Study Group</s1><s3>USA</s3></fA17><fA20><s1>233-248</s1></fA20><fA21><s1>2005</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>2052</s2><s5>354000138405420060</s5></fA43><fA44><s0>0000</s0><s1>© 2005 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>53 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>05-0376425</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>The Journal of infectious diseases</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Background. The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period. Methods. We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank. Results. In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen. Conclusion. We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970.</s0></fC01><fC02 i1="01" i2="X"><s0>002A05</s0></fC02><fC02 i1="02" i2="X"><s0>002B05</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Hong Kong</s0><s2>NG</s2><s5>05</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Hong Kong</s0><s2>NG</s2><s5>05</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Hong Kong</s0><s2>NG</s2><s5>05</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Microbiologie</s0><s5>06</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Microbiology</s0><s5>06</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Microbiología</s0><s5>06</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Infection</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Infection</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Infección</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Grippe A</s0><s5>14</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Influenza A</s0><s5>14</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Gripe A</s0><s5>14</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Chine</s0><s2>NG</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>China</s0><s2>NG</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>China</s0><s2>NG</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Asie</s0><s2>NG</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Asia</s0><s2>NG</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Asia</s0><s2>NG</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Virose</s0></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Viral disease</s0></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Virosis</s0></fC07><fN21><s1>262</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 05-0376425 INIST</NO><ET>Multinational impact of the 1968 Hong Kong influenza pandemic : Evidence for a smoldering pandemic</ET><AU>VIBOUD (Cécile); GRAIS (Rebecca F.); LAFONT (Bernard A. P.); MILLER (Mark A.); SIMONSEN (Lone)</AU><AF>Fogarty International Center, National Institutes of Health/Bethesda, Maryland/Etats-Unis (1 aut., 2 aut., 4 aut.); National Institute of Allergy and Infectious Diseases, National Institutes of Health/Bethesda, Maryland/Etats-Unis (3 aut., 5 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2005; Vol. 192; No. 2; Pp. 233-248; Bibl. 53 ref.</SO><LA>Anglais</LA><EA>Background. The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period. Methods. We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank. Results. In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen. Conclusion. We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970.</EA><CC>002A05; 002B05</CC><FD>Hong Kong; Microbiologie; Infection; Grippe A</FD><FG>Chine; Asie; Virose</FG><ED>Hong Kong; Microbiology; Infection; Influenza A</ED><EG>China; Asia; Viral disease</EG><SD>Hong Kong; Microbiología; Infección; Gripe A</SD><LO>INIST-2052.354000138405420060</LO><ID>05-0376425</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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