# 4271
After four years of blogging about influenza – whether it be human, swine, or avian – very little surprises me. I’m used to having yesterday’s assumptions trashed by today’s studies.
And I’m resigned to the possibility that what we think we learned today may be overturned next week or next month.
For the past five years or so the assumption has been that the 1918 H1N1 virus likely arose from an avianlike flu strain that jumped from some unidentified host reservoir nearly simultaneously to humans and swine.
While suggestive of an avian origin, that has never been proven. This from a paper published in the CDC’s EID journal in 2006.
1918 Influenza: the Mother of All Pandemics
EID Journal Jan 2006
Jeffery K. Taubenberger and David M. Morens
(Excerpts)
The 1918 influenza pandemic had another unique feature, the simultaneous (or nearly simultaneous) infection of humans and swine. The virus of the 1918 pandemic likely expressed an antigenically novel subtype to which most humans and swine were immunologically naive in 1918 (12,20).
Recently published sequence and phylogenetic analyses suggest that the genes encoding the HA and neuraminidase (NA) surface proteins of the 1918 virus were derived from an avianlike influenza virus shortly before the start of the pandemic and that the precursor virus had not circulated widely in humans or swine in the few decades before (12,15,24).
More recent analyses of the other gene segments of the virus also support this conclusion. Regression analyses of human and swine influenza sequences obtained from 1930 to the present place the initial circulation of the 1918 precursor virus in humans at approximately 1915–1918 (20).
Thus, the precursor was probably not circulating widely in humans until shortly before 1918, nor did it appear to have jumped directly from any species of bird studied to date (19). In summary, its origin remains puzzling.
Today, several news outlets are carrying details of a study which appears in the February, 2010 edition of the Journal of General Virology, entitled:
1918 and 2009 H1N1 influenza viruses are not pathogenic in birds
Shawn Babiuk1,2, Randy Albrecht3, Yohannes Berhane1, Peter Marszal1, Jürgen A. Richt4, Adolfo García-Sastre3,5,6, John Pasick1 and Hana Weingartl1,7
Typical of the coverage is this, from Medical News Today.
1918 And 2009 H1N1 Flu Probably Not Spread By Birds
Article Date: 20 Jan 2010 - 5:00 PSTThe two strains of the H1N1 influenza virus responsible for the 1918 and 2009 global flu pandemics do not cause disease in birds. The results of the study, published in the February issue of the Journal of General Virology, also show it is unlikely that birds played a role in the spread of the H1N1 virus in these pandemics.
Scientists from the Canadian Food Inspection Agency's National Centre for Foreign Animal Disease (NCFAD) in Winnipeg, Canada, together with collaborators in the USA, injected the 2009 and 1918 H1N1 virus strains individually into chickens. None developed flu symptoms or showed any signs of tissue damage up to18 days later, although about half the chickens developed antibodies against the 1918 H1N1 virus showing limited infection. The 1918 H1N1 virus also did not cause disease in ducks.
The origin of the 1918 H1N1 virus is unknown and despite its genetic similarity to avian influenzas, the results of this study show it is unlikely to have jumped the species barrier from chickens to humans.
I can almost hear you say . . . `Yes, but . . . what about the turkey flocks infected with novel H1N1?’
For the answers to that, and other hanging questions, we can go to the study itself. First from the Abstract:
ABSTRACT
The susceptibility of chickens to both 1918 and 2009 H1N1 influenza virus was evaluated. The intravenous pathogenicity index of 1918 and 2009 H1N1 viruses in chickens was 0. Chickens did not develop clinical signs following experimental inoculation simulating natural infection. No gross pathological changes were observed in any tissues of chickens between 2 and 18 days post-infection (p.i.) and viral RNA was not detected by real-time RT-PCR in mucosal secretions or tissues. Seroconversion was not detected in any of the chickens following inoculation with H1N1 2009 virus, whereas half the chickens developed influenza-specific antibodies at 28 days p.i. with 1918 influenza, suggesting limited infection.
Viral RNA was detected by real-time RT-PCR in mallard ducks following inoculation with 1918 influenza virus at 3 days p.i. in cloacal swabs, but not in tissues, and all ducks seroconverted by 28 days p.i.
Both 1918 and 2009 H1N1 influenza viruses behave as LPAI in gallinaceous poultry.
So . . . while the title of the study, and the mainstream press reports, refer to `birds’ . . . in truth this study only looked a chickens, mallard ducks, and gallinaceous poultry.
Gallinaceous poultry refers to heavy-bodied ground-feeding domestic or game birds such as grouse, turkeys, pheasants and quail.
According to this study, chickens are not particularly susceptible to the novel H1N1 virus, and only marginally to the 1918 strain.
Mallard ducks were apparently susceptible to the 1918 virus, in that they all seroconverted within 28 days post infection.
But both chickens and ducks were asymptomatic.
In Turkeys and other gallinaceous poultry, infected birds experienced mild LPAI symptoms, such as a reduction in egg production.
Does all of this mean that birds were not the source of the 1918 H1N1 virus?
No. And the authors make that point towards the end of their paper.
In any case, our results argue that the 1918 influenza virus, despite its high virulence in mice, ferrets, macaques and humans and its genotypic similarities to avian influenza viruses, replicates poorly in chickens and mallard ducks and therefore was unlikely to have made the direct jump from domestic chicken or mallard duck to humans.
The 1918 influenza might then have originated from an ‘unknown’ avian or other source (Reid et al., 2004) before probably acquiring several adaptive changes through mutation or even reassortment processes with other influenza viruses.
The good news here is that those species of birds most likely to come in close contact with humans (chickens, ducks, turkeys) appear to be poor hosts for the novel H1N1 virus, and (for now) are probably not a factor in the spread of the virus.
As far as the origins of the 1918 pandemic virus goes?
Well . . . this is another piece of the puzzle, but not the final solution.
