L’étude de la structure génétique du H1N1 montre qu’il est l’héritier de trois souches provenant d’Amérique, d’Europe et d’Asie. Les auteurs de cette publication s’interrogent sur le lieu où cette recombinaison a pu se produire.
La première hypothèse est celle d’un élevage de porcs, avec un transport des souches via les animaux eux-mêmes ou les oiseaux.
La seconde est celle d’une erreur de manipulation dans un laboratoire de recherche ou lors de la production des vaccins animaux.
From where did the 2009 ’swine-origin’ influenza A virus (H1N1) emerge ?
Adrian J Gibbs , John S Armstrong and Jean C Downie, 24 November 2009
The swine-origin influenza A (H1N1) virus that appeared in 2009 and was first found in human beings in Mexico, is a reassortant with at least three parents. Six of the genes are closest in sequence to those of H1N2 ’triple-reassortant’ influenza viruses isolated from pigs in North America around 1999-2000.
Its other two genes are from different Eurasian ’avian-like’ viruses of pigs ; the NA gene is closest to H1N1 viruses isolated in Europe in 1991-1993, and the MP gene is closest to H3N2 viruses isolated in Asia in 1999-2000. The sequences of these genes do not directly reveal the immediate source of the virus as the closest were from isolates collected more than a decade before the human pandemic started.
The three parents of the virus may have been assembled in one place by natural means, such as by migrating birds, however the consistent link with pig viruses suggests that human activity was involved. We discuss a published suggestion that unsampled pig herds, the intercontinental live pig trade, together with porous quarantine barriers, generated the reassortant.
We contrast that suggestion with the possibility that laboratory errors involving the sharing of virus isolates and cultured cells, or perhaps vaccine production, may have been involved. Gene sequences from isolates that bridge the time and phylogenetic gap between the new virus and its parents will distinguish between these possibilities, and we suggest where they should be sought.
It is important that the source of the new virus be found if we wish to avoid future pandemics rather than just trying to minimize the consequences after they have emerged. Influenza virus is a very significant zoonotic pathogen. Public confidence in influenza research, and the agribusinesses that are based on influenza’s many hosts, has been eroded by several recent events involving the virus. Measures that might restore confidence include establishing a unified international administrative framework coordinating surveillance, research and commercial work with this virus, and maintaining an registry of all influenza isolates.
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The “laboratory error” theory.
We note that influenza viruses survive well in virus laboratories, that laboratories are not subject to routine surveillance, and that there are probably many laboratories in the world that share and propagate a range of swine influenza viruses from different sources and continents, and also share and use immortalized lines of cultured cells.
The viruses are used for research, diagnostic tests and for making vaccines, and the cells are used for propagating the viruses. Thus if S-OIV [ Swine-Origin Influenza Virus -ndlr ] had been generated by laboratory activity, when one host was simultaneously infected with strains from the different parental lineages, this would explain most simply why S-OIV’s genes had escaped surveillance for over a decade, and how viruses last sampled in North America, Europe and Asia became assembled in one place and generated a reassortant.
So what sort of laboratory event might produce mixed infections with different strains of influenza, and thereby generate S-OIV ? The simplest is that S-OIV is a reassortant produced during research. There is also the possibility that it was generated during the production of multivalent vaccines. Multivalent ‘killed’ vaccines are mixtures of virions that have been grown in hen’s eggs and then chemically sterilized. Thus a reassortant might be produced if insufficient sterilant, usually formaldehyde or propiolactone, is added to the virion mixture.
The live mixture could then infect pigs ‘vaccinated’ with it, and the growing viruses could reassort, infect piggery staff and hence spread to the broader human population. Finally, it is possible that serially passaged cells, such as the Madin-Darby canine kidney (MDCK) cells now widely used in influenza laboratories, became latently and serially infected with different strains of influenza as a result of lax laboratory practices. This process could generate reassortants, and infect staff.
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Circumstantial Evidence
There are clear historical precedents for most of the events described in the above scenarios. Viruses do ‘escape’ from laboratories, even high security facilities. The H1N1 influenza lineage that circulated in the human population for four decades after the 1918 Spanish influenza epidemic, disappeared during the 1957 Asian influenza pandemic, was absent for two decades, but then reappeared in 1977.
Gene sequences of the 1977 isolate and others collected in the 1950s were almost identical, indicating that the virus had not replicated and evolved in the interim, and had probably been held in a laboratory freezer between 1950 and 1977 and ‘escaped’ during passaging.
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Bloomberg Scientist Repeats Swine Flu Lab-Escape Claim in Published Study
Adrian Gibbs, the virologist who said in May that swine flu may have escaped from a laboratory, published his findings today, renewing discussion about the origins of the pandemic virus.
The new H1N1 strain, which was discovered in Mexico and the U.S. in April, may be the product of three strains from three continents that swapped genes in a lab or a vaccine-making plant, Gibbs, and fellow Australian scientists wrote in Virology Journal. The authors analyzed the genetic makeup of the virus and found its origin could be more simply explained by human involvement than a coincidence of nature.
