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Was the 1918 pandemic a result of a swine virus or avian virus?

A

AlexanderSJones

Well-known member
How is it apples and oranges?

1918 was a swine virus that came in multiple waves. We are already at a 0.4% case fatality rate -- this is comparable to the 1957 pandemic. There are probably not many SNPs required to increase the H1N1 case fatality rate to the level of 1918 (2.5%).

The only questions to me, really, are:

A) Did the toddler die of H1N1?
B) If so, what is the genome sequence?
 
Re: Queens tot susoected to be second swine flu death in New York City

Re: Queens tot susoected to be second swine flu death in New York City

AlexanderSJones said:
How is it apples and oranges?

1918 was a swine virus that came in multiple waves. We are already at a 0.4% case fatality rate -- this is comparable to the 1957 pandemic. There are probably not many SNPs required to increase the H1N1 case fatality rate to the level of 1918 (2.5%).

The only questions to me, really, are:

A) Did the toddler die of H1N1?
B) If so, what is the genome sequence?
Click to expand...

But - until yesterday - 1918 H1N1 was an fully avian influenza virus adapted to humans...
 
Re: Queens tot suspected to be second swine flu death in New York City

Re: Queens tot suspected to be second swine flu death in New York City

I subscribe to the school of thought that 1918 was a swine, not avian virus. I believe Dr. Niman holds a similar view.
 
Re: Queens tot suspected to be second swine flu death in New York City

Re: Queens tot suspected to be second swine flu death in New York City

AlexanderSJones said:
I subscribe to the school of thought that 1918 was a swine, not avian virus. I believe Dr. Niman holds a similar view.
Click to expand...

After tons of papers during last six years I was nearly sure that the question was finally cleared: an avian influenza virus that adapted to human host.

If now, after that, suddenly, 1918 virus has became a swine flu - well - I will throw out the window all these papers.
 
Re: Queens tot suspected to be second swine flu death in New York City

Re: Queens tot suspected to be second swine flu death in New York City

Well it's still somewhat of a contentious topic.

1: Mol Phylogenet Evol. 2008 Jun;47(3):1100-10. Epub 2008 Feb 14.Click here to read Links
Origin of the 1918 Spanish influenza virus: a comparative genomic analysis.
Vana G, Westover KM.

Department of Biology, Winthrop University, Rock Hill, SC 29733, USA.

To test the avian-origin hypothesis of the 1918 Spanish influenza virus we surveyed influenza sequences from a broad taxonomic distribution and collected 65 full-length genomes representing avian, human and "classic" swine H1N1 lineages in addition to numerous other swine (H1N2, H3N1, and H3N2), human (H2N2, H3N2, and H5N1), and avian (H1N1, H4N6, H5N1, H6N1, H6N6, H6N8, H7N3, H8N4, H9N2, and H13N2) subtypes. Amino acids from all eight segments were concatenated, aligned, and used for phylogenetic analyses. In addition, the genes of the polymerase complex (PB1, PB2, and PA) were analyzed individually. All of our results showed the Brevig-Mission/1918 strain in a position basal to the rest of the clade containing human H1N1s and were consistent with a reassortment hypothesis for the origin of the 1918 virus. Our genome phylogeny further indicates a sister relationship with the "classic" swine H1N1 lineage. The individual PB1, PB2, and PA phylogenies were consistent with reassortment/recombination hypotheses for these genes. These results demonstrate the importance of using a complete-genome approach for addressing the avian-origin hypothesis and predicting the emergence of new pandemic influenza strains.

http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
 
Re: Queens tot suspected to be second swine flu death in New York City

Re: Queens tot suspected to be second swine flu death in New York City

AlexanderSJones said:
Well it's still somewhat of a contentious topic.

1: Mol Phylogenet Evol. 2008 Jun;47(3):1100-10. Epub 2008 Feb 14.Click here to read Links
Origin of the 1918 Spanish influenza virus: a comparative genomic analysis.
Vana G, Westover KM.

Department of Biology, Winthrop University, Rock Hill, SC 29733, USA.

To test the avian-origin hypothesis of the 1918 Spanish influenza virus we surveyed influenza sequences from a broad taxonomic distribution and collected 65 full-length genomes representing avian, human and "classic" swine H1N1 lineages in addition to numerous other swine (H1N2, H3N1, and H3N2), human (H2N2, H3N2, and H5N1), and avian (H1N1, H4N6, H5N1, H6N1, H6N6, H6N8, H7N3, H8N4, H9N2, and H13N2) subtypes. Amino acids from all eight segments were concatenated, aligned, and used for phylogenetic analyses. In addition, the genes of the polymerase complex (PB1, PB2, and PA) were analyzed individually. All of our results showed the Brevig-Mission/1918 strain in a position basal to the rest of the clade containing human H1N1s and were consistent with a reassortment hypothesis for the origin of the 1918 virus. Our genome phylogeny further indicates a sister relationship with the "classic" swine H1N1 lineage. The individual PB1, PB2, and PA phylogenies were consistent with reassortment/recombination hypotheses for these genes. These results demonstrate the importance of using a complete-genome approach for addressing the avian-origin hypothesis and predicting the emergence of new pandemic influenza strains.

http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Click to expand...


<table width="100%" border="0" cellpadding="0" cellspacing="3"><tbody><tr><td class="content-cell" valign="top">Characterization of the 1918 ?Spanish? influenza virus neuraminidase gene
Ann H. Reid,<sup>*</sup> Thomas G. Fanning, Thomas A. Janczewski, and Jeffery K. Taubenberger
Division of Molecular Pathology, Department of Cellular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000
<sup>*</sup>To whom reprint requests should be addressed at: Department of Cellular Pathology, Armed Forces Institute of Pathology, 14th Street and Alaska Avenue NW, Washington, DC 20306-6000. E-mail: reid@afip.osd.mil<script type="text/javascript" language="JavaScript"><!-- try{initUnObscureEmail ("e_id498045", '' + reverseAndReplaceString('lim.dso.pifa/ta/dier', '/at/','@') + '')}catch(e){} //--></script>.
Communicated by Edwin D. Kilbourne, New York Medical College, Madison, CT

Received January 4, 2000; Accepted March 29, 2000.
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This article has been cited by other articles in PMC.


</td></tr><tr valign="top"><td class="sidebar-cell" width="145"> </td><td class="content-cell">Abstract
<!--article-meta-->The ?Spanish? influenza pandemic of 1918 was characterized by exceptionally high mortality, especially among young adults. The surface proteins of influenza viruses, hemagglutinin and neuraminidase, play important roles in virulence, host specificity, and the human immune response. The complete coding sequence of hemagglutinin was reported last year. This laboratory has now determined the complete coding sequence of the neuraminidase gene of the 1918 virus. Influenza RNA fragments were isolated from lung tissue of three victims of the 1918 flu; complete sequence was generated from A/Brevig Mission/1/18, with confirmatory sequencing carried out on A/South Carolina/1/18 and A/New York/1/18. The 1918 neuraminidase gene sequence was compared with other N1 subtype neuraminidase genes, including 9 N1 strains newly sequenced for this study. The 1918 neuraminidase shares many sequence and structural characteristics with avian strains, including the conserved active site, wild-type stalk length, glycosylation sites, and antigenic sites. Phylogenetically, the 1918 neuraminidase gene appears to be intermediate between mammals and birds, suggesting that it was introduced into mammals just before the 1918 pandemic.

</td></tr></tbody></table>
 
Re: Queens tot suspected to be second swine flu death in New York City

Re: Queens tot suspected to be second swine flu death in New York City

90% of the 1918 polymorphismsmcan be found in two isolates, human H1N1 (WSN/33) and swine H1N1 (swine/iowa/30). It was a recombinant between human and swine h1n1 in all 8 gene segments.
 
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