In a recent article in ” The New England Journal of Medicine” by Shanta M. Zimmer, M.D. and Donald S. Burke, M.D. entitled “Historical Perspective — Emergence of Influenza A (H1N1) Viruses” http://content.nejm.org/cgi/content/full/361/3/279

They break down the history of the virus ( Sorry YouConspiracyTheoristsAreRetards & spectator )

A couple of things fronm the paper to enlighten you guys:

Extinction of Human H1N1 Virus (1957):

Influenza A (H1N1) abruptly disappeared from humans in 1957 and was replaced by a new reassortant virus that combined genes from the H1N1 strain and an avian virus. This new influenza A (H2N2) strain contained three new segments from the avian source and maintained the other five segments from the H1N1 strain of 1918 lineage.17 After this pandemic subtype emerged, human influenza A (H1N1) was not detected again until 1977.18 Reasons for the complete disappearance of this strain in 1957 are not clear, but it is likely that high levels of existing homologous immunity, coupled with a burst of heterologous immunity from the new H2N2 strain, were sufficient to eliminate the virus.

H1N1 Reemergence in Humans (1977):

Even though human influenza A (H1N1) virus had not circulated since 1957 and the swine influenza A (H1N1) virus that had been identified at Fort Dix did not extend outside the base, in November 1977, the H1N1 strain reemerged in the former Soviet Union, Hong Kong, and northeastern China. This strain affected primarily young people in a relatively mild presentation.18,30 Careful study of the genetic origin of the virus showed that it was closely related to a 1950 strain but dissimilar to influenza A (H1N1) strains from both 1947 and 1957. This finding suggested that the 1977 outbreak strain had been preserved since 1950.30 The reemergence was probably an accidental release from a laboratory source in the setting of waning population immunity to H1 and N1 antigens.19,31

Conclusions:

The history of influenza A (H1N1) virus is punctuated by frequent, sporadic cross-species transmissions from swine to humans. Although the sporadically transmitted swine viruses are sufficiently pathogenic in humans to cause clinically apparent disease, they are rarely transmitted among humans. Exposure and infection are necessary but not sufficient for a new epidemic virus to emerge; the virus must also adapt and transmit.12 The one prominent exception to the general rule that these swine viruses are not transmitted among humans was the outbreak at Fort Dix. This virus was never transmitted beyond the military installation, probably because the intrinsic transmissibility of the virus was simply too low. Yet the global response to this outbreak was forceful, especially given that the outbreak self-quenched. The decision to mass-vaccinate the U.S. population resulted in the unfortunately large cluster of Guillain–Barré cases. Perhaps an even more serious consequence was the accidental release of human-adapted influenza A (H1N1) virus from a research study, with subsequent resurrection and global spread of this previously extinct virus, leading to what could be regarded as a “self-fulfilling prophecy” epidemic. The 1998 triple reassortant influenza A (H1N1) swine virus has shown what appears to be a proclivity to jump the species barrier and cause swine-to-human infections.

Everything is documented in the article. When we seek the truth, it will appear.

Three separate articles offer an explanation for the origin of H1N1 (Brockwell-Staats et al., 2009; Kingsford et al., 2009; Smith et al., 2009). The explanation is based on facts, including gene sequences of previously known influenza viruses. While it is possible that H1N1 was engineered, there is no direct evidence of this. The best explanation for H1N1 is a natural origin.

One virologist, Adrian Gibbs, hypothesized that H1N1 escaped from a lab. He has stated that he is uncertain of this and that it is simply a plausible hypothesis. The WHO has responded that the hypothesis does not stand to scrutiny (Hitt, 2009).

Brockwell-Staats C, Webster RG, Webby RJ. (2009) Diversity of Influenza Viruses in Swine and the Emergence of a Novel Human Pandemic Influenza A (H1N1). Influenza Other Respi Viruses. 3: 207 – 213.
[PMID: 19768134]

Hitt E. (May 14, 2009) Novel H1N1 Flu a Naturally Circulating Virus, Not From a Laboratory. Medscape Medical News.
[http://www.medscape.com/viewarticle/702862]

Kingsford C, Nagarajan N, Salzberg SL. (2009) 2009 Swine-origin influenza A (H1N1) resembles previous influenza isolates. PLoS One. 4: e6402.
[http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0006402]

Smith GJ, Vijaykrishna D, Bahl J, Lycett SJ, Worobey M, Pybus OG, Ma SK, Cheung CL, Raghwani J, Bhatt S, Peiris JS, Guan Y, Rambaut A. (2009) Origins and evolutionary genomics of 2009 swine-origin H1N1 influenza A epidemic. Nature. 459: 1122 – 1125.
[http://www.nature.com/nature/journal/v459/n7250/pdf/nature08182.pdf]

——–

A simple summary of the three articles offering an explanation for 2009/H1N1′s natural origin follows.

Influenza A virus genome consists of 8 negative sense ssRNA segments: M, NA, PB1, PB2, PA, NP, NS and HA. Influenza viruses change by reassortment, which occurs when two different influenza viruses infect one cell and RNA segments are mixed. Pigs are thought to be reassortment vessels for influenza because they can be infected by swine, avian and mammalian strains (Webster et al., 1992).

Pandemic 2009/H1N1 resulted through reassortment between Eurasian swine H1N1 (ES-H1N1) and triple reassortment swine H1N2 (TRS-H1N2). The M and NA segments came from the ES-H1N1 and other 6 came from TRS-H1N2.

TRS-H1N2 has been circulating in North America since 1998. It has PB1 and NA segments from human H3N2 influenza; PA and PB2 segments from avian influenza; NP, M, NS and HA segments from classical H1N1 swine influenza. When ES-H1N1 and TRS-H1N2 reassorted, the M and NA segments from H1N1 were packaged with the six other segments from H1N2. 2009/H1N1 is this new 2+6 ‘package’ of gene segments.

Webster RG, Bean WJ, Gorman OT, Chambers TM, Kawaoka Y. (1992) Evolution and ecology of influenza A viruses. Microbiol Rev. 56: 152 – 179.
[http://mmbr.asm.org/cgi/reprint/56/1/152.pdf]

Could you please explain that because NOTHING on your site makes me see why you could think that all signs point to this being an engineered virus? I mean seriously, you haven’t offered a single fact that directly points to a genetically engineered origin but you’re trying to say that “all signs” point to that? You haven’t made a coherent argument to support that assertion and I think it’s irresponsible of you to jump to such conclusions.

Three separate articles offer an explanation for the origin of H1N1 (Brockwell-Staats et al., 2009; Kingsford et al., 2009; Smith et al., 2009). The explanation is based on facts, including gene sequences of previously known influenza viruses. While it is possible that H1N1 was engineered, there is no direct evidence of this. The best explanation for H1N1 is a natural origin.

One virologist, Adrian Gibbs, hypothesized that H1N1 escaped from a lab. He has stated that he is uncertain of this and that it is simply a plausible hypothesis. The WHO has responded that the hypothesis does not stand to scrutiny (Hitt, 2009).

Brockwell-Staats C, Webster RG, Webby RJ. (2009) Diversity of Influenza Viruses in Swine and the Emergence of a Novel Human Pandemic Influenza A (H1N1). Influenza Other Respi Viruses. 3: 207 – 213.
[PMID: 19768134]

Hitt E. (May 14, 2009) Novel H1N1 Flu a Naturally Circulating Virus, Not From a Laboratory. Medscape Medical News.
[http://www.medscape.com/viewarticle/702862]

Kingsford C, Nagarajan N, Salzberg SL. (2009) 2009 Swine-origin influenza A (H1N1) resembles previous influenza isolates. PLoS One. 4: e6402.
http://www.plosone.org/article.....ne.0006402

Smith GJ, Vijaykrishna D, Bahl J, Lycett SJ, Worobey M, Pybus OG, Ma SK, Cheung CL, Raghwani J, Bhatt S, Peiris JS, Guan Y, Rambaut A. (2009) Origins and evolutionary genomics of 2009 swine-origin H1N1 influenza A epidemic. Nature. 459: 1122 – 1125.
[http://www.nature.com/nature/journal/v459/n7250/pdf/nature08182.pdf]

——–

A simple summary of the three articles offering an explanation for 2009/H1N1′s natural origin follows.

Influenza A virus genome consists of 8 negative sense ssRNA segments: M, NA, PB1, PB2, PA, NP, NS and HA. Influenza viruses change by reassortment, which occurs when two different influenza viruses infect one cell and RNA segments are mixed. Pigs are thought to be reassortment vessels for influenza because they can be infected by swine, avian and mammalian strains (Webster et al., 1992).

Pandemic 2009/H1N1 resulted through reassortment between Eurasian swine H1N1 (ES-H1N1) and triple reassortment swine H1N2 (TRS-H1N2). The M and NA segments came from the ES-H1N1 and other 6 came from TRS-H1N2.

TRS-H1N2 has been circulating in North America since 1998. It has PB1 and NA segments from human H3N2 influenza; PA and PB2 segments from avian influenza; NP, M, NS and HA segments from classical H1N1 swine influenza. When ES-H1N1 and TRS-H1N2 reassorted, the M and NA segments from H1N1 were packaged with the six other segments from H1N2. 2009/H1N1 is this new 2+6 ‘package’ of gene segments.

Webster RG, Bean WJ, Gorman OT, Chambers TM, Kawaoka Y. (1992) Evolution and ecology of influenza A viruses. Microbiol Rev. 56: 152 – 179.
[http://mmbr.asm.org/cgi/reprint/56/1/152.pdf]