By Wayne Madsen

A virologist who has been researching the A/H1N1 virus has concluded after months of research that the ”novel” influenza was re-assorted in a laboratory from eight genes consisting of avian, swine and human type influenza A virus.

The scientist does not believe, based on intensive laboratory research of the A/H1N1 virus, that its sudden appearance in Mexico this past spring was a natural occurrence.

The reassortment of viruses occurs when one or more complete genes are exchanged enabling the virus to adapt to a new host. An example is when the avian virus switches gene with a human virus. In the case of A/H1N1, three genes were exchanged, from avian, swine, and human influenza viruses, resulting in the ressortant virus now expected to launch another deadly wave of infections in early October.

There are also signs that adaptation leading to mutation has occurred in the A/H1N1 strain. Several cases of mutated A/H1N1 have been reported from around the globe, rendering treatment with anti-A/H1N1 drugs and A/H1N1 vaccines ineffective.

Adaptation takes place when a small change takes place in the virus and sometimes that can be one amino acid alteration. The adaptation permits the virus to thrive in its new host. A/H1N1 is believed to be a laboratory strain because a specific amino acid was discovered that appears to have made several passages in eggs. The vaccine industry usually amplifies viruses by isolating them in eggs and after several passages, the mutation can be discovered.

The mutation of A/H1N1 has been discovered by our virologist source to have been more rapid than is naturally possible. The following is what was described in scientific terms about the rate of mutation of A/H1N1:

“Mutation takes time to occur, up to the rate of amino acid substitution. For example, for HA gene, or “duck virus,” HA has a substitution rate about 3 x 10e-4 per site per year which is slower compare to human and swine HA (about 10e-3 per site per year). If the total nucleotide number in influenza A virus HA is 1,700, then it takes three years for making a single change in the duck virus, or 1.7 year in the case of human and swine virus.”

The natural rate of mutation for a complete gene mutation, according to the virologist, takes “thousand of years to be established.”

As far as the reassortant A/H1N1 virus is concerned, there is a fear that a human was used as a laboratory “guinea pig” to permit the exchange of genes between humans, pigs, and fowl. The reasoning is that an individual was infected by avian, human and swine virus simultaneously, and the viruses exchanged genes inside the individual’s body, creating a new virus having mixed genes and then rapidly spreading to others.

Herein lies the suspicions concerning the purposeful creation of A/H1N1 and its infection of a human host.

WMR’s virologist source stated, “The host should have efficient receptor for those three different derived hosts. So far, human virus tends to infect humans, because it is suited to a human receptor. Avian virus tends to infect birds, because it is suited to bird receptors. Pigs have both human and avian type receptors, so it is believed that pig serves as the ‘mixing vessel.’ However, some researchers tried to prove the ‘mixing vessel’ theory by trying to infect pigs with human and avian viruses to create a reassortant virus.”

The test involving the infection of pigs with reassortant human and avian viruses failed.

While it is common for pigs to become infected with human and avian viruses, there are no reports that pigs shed the reassortant A/H1N1 virus and infected new hosts, either human or bird.

What is known is that the first A/H1N1 virus was found in a human. Although some pigs and turkeys were infected with the A/H1N1 virus by farm workers, there is no evidence that the opposite occured.

Reassortant genes also require ancestor viruses. According to the virologist, “If you check the phylogenetic tree, it shows the NA and M genes derived from avian virus, PB1 from human H3N2; other genes (PB2, PA, HA, NP, NS) from swine triple reassortant, swine H1N2 and Eurasian swine (H1N1/H3N2). The triple reassortant swine actually derived from human H3N2 which infected pigs, and has been circulating in North America for at least 20 years. When people say it is ‘swine virus,’ it’s actually human virus.”

It has also been discovered that suspected ancestor viruses are coming from old isolates. The NA gene comes from a 1996-2001 isolate, the M gene from 1990-1993 isolates, and the others even older, somewhere between 1979 to 1980’s isolates. The consensus virologist community contends that the A/H1N1 virus has been in existence for over 20 years without ever being detected. WMR’s virologist states that it is impossible for a virus existing for 20 years without being detected given the amount of virus medical surveillance that takes place around the world.

The virologist has not detected any evidence of 1918 influenza RNA/DNA in A/H1N1. However, the 1918 flu, like A/H1N1, began in a first wave in the spring and came back with a vengeance in October. The 1918 flu killed an estimated 50 million people around the world. Although no genetic evidence of a link to 1918 flu has been discovered by the virologist, the same scientist who has conducted research into A/H1N1 and may have received DNA samples from the buried corpse of an Inuit woman in Fort Brevig, Alaska, who died of the pandemic in 1918 is also financially linked to an A/H1N1 vaccine firm.

The virologist has asked an alarming question about A/H1N1,”How can you mix avian, human and pig virus at one time? The viruses must have come from Europe, America and Asia, without any detection?”

The virologist adds, “The virus emerged suddenly in Mexico. I can’t explain how. I wish I could. For me as a virologist, it’s impossible . . . on the other hand, technology can create any kind of virus you want.”