Our seasonal flu might be a direct descendant of the 1918 'Spanish flu'

Publicly released:
International
By Otis Historical Archives, National Museum of Health and Medicine - Emergency hospital during influenza epidemic (NCP 1603), National Museum of Health and Medicine.https://www.buckscountycouriertimes.com/news/20190923/mxfctter-museum-to-mark-historic-influenza-pandemic/1, Public Domain, https://commons.wikimedia.org/w/index.php?curid=25513204
By Otis Historical Archives, National Museum of Health and Medicine - Emergency hospital during influenza epidemic (NCP 1603), National Museum of Health and Medicine.https://www.buckscountycouriertimes.com/news/20190923/mxfctter-museum-to-mark-historic-influenza-pandemic/1, Public Domain, https://commons.wikimedia.org/w/index.php?curid=25513204

Our seasonal version of the H1N1 flu virus might have had a much more sinister origin, after international researchers discovered that it could be a direct descendant of the 1918 influenza strain that caused a global pandemic and killed between 50 and 100 million people. The team worked this out by analysing lung specimens from historical archives collected between 1901 and 1931. They say that the lungs had specific genes, that when mapped against our current H1N1 strain, suggests that they contained a genomic ancestor to our yearly flu.

Media release

From: Springer Nature

Seasonal H1N1 flu may be descended from 1918 pandemic strain *PRESS BRIEFING* 


The seasonal H1N1 flu virus may be a direct descendant of the 1918 influenza strain that caused a global flu pandemic, suggests a paper published in Nature Communications. The findings are based on the genomic analysis of samples that were collected in Europe during the 1918 pandemic.

The 1918 pandemic is estimated to have cost the lives 50 to 100 million people worldwide. Our understanding of its spread and timing is based on historical and medical records, which indicate its peak occurred in the autumn of 1918 and it continued through to winter 1919. However, it was only in the 1930s that it was confirmed to be of viral origin, while more recent research has since suggested the virus was an influenza A virus (IAV) of the H1N1 subtype. Genomic analysis of the 1918 virus is difficult due to the rarity of viral sequences from the time period.

Sébastien Calvignac-Spencer and colleagues analysed 13 lung specimens from different individuals stored in historical archives of museums in Germany and Austria, collected between 1901 and 1931, which included 6 samples collected in 1918 and 1919. From these they were able to sequence two partial genomes collected in Berlin in June 1918 and a complete genome collected in Munich in 1918. The authors suggest that the genomic diversity of the samples is consistent with a combination of local transmission and long-distance dispersal events. They compared genomes from before and after the pandemic’s peak and suggest there is a variation in the nucleoprotein gene which is associated with resistance to antiviral responses and could have enabled the virus’ adaptation to humans. The authors also conducted molecular clock modelling, a method which allows evolutionary timescales to be estimated, and suggest that all genomic segments of the seasonal H1N1 flu could be directly descended from the initial 1918 pandemic strain. This contradicts other hypotheses which suggest the seasonal virus emerged through reassortment (the exchange of genomic segments between different viruses).

The authors highlight that samples are still scarce but the insights gained here into the evolution and progress of the 1918 flu pandemic show the value of prospecting historical archives.
 

Journal/
conference:
Nature Communications
Research:Paper
Organisation/s: Robert Koch Institute, Berlin, Germany
Funder: B.V. and S.L. were supported by postdoctoral fellowship grants of the Research Foundation–Flanders (Fonds voor Wetenschappelijk Onderzoek, 12U7121N and 12R4718N, respectively). M.T.P.G. acknowledges Danish National Research Foundation Award DNRF143 for funding. This work was funded in part by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases of the NIH (D.M.M. and J.K.T.). MAS was supported by US National Institutes of Health grants HG006139 and AI135995. M.W. was supported by the Bill and Melinda Gates Foundation (INV- 004212) and the David and Lucile Packard Foundation. VJS was supported by the University of Zurich’s University Research Priority Program “Evolution in Action: From Genomes to Ecosystems”. The research leading to these results has received funding from the European Research Council under the European Union’s Horizon 2020 research and innovation program (grant agreement no. 725422-ReservoirDOCS) and from the European Union’s Horizon 2020 project MOOD (grant agreement no. 874850). The Artic Network receives funding from the Wellcome Trust through project 206298/Z/17/Z. PL acknowledges support by the Research Foundation - Flanders (‘Fonds voor Wetenschappelijk Onderzoek - Vlaanderen’, G0D5117N and G0B9317N). This project was also supported by a grant to SCS from the National Research Platform for Zoonoses (Federal Ministry of Education and Research, 01KI1714), and in part by a grant to TW from the Deutsche Forschungsgemeinschaft (Transregio 84, project B2).
Media Contact/s
Contact details are only visible to registered journalists.