A/H1N1 was re-assorted in a lab

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 passage 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 human, 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 but 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 twenty years without ever being detected. WMR's virologist states that it is impossible for a virus existing for twenty 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."

Hybrid A/H1N1 flu tied to genetic trigger for larger, mutated version

WMR previously reported on the genetic manipulation of the 1918 flu from tissue extracted from an Inuit woman who died from the pandemic in Alaska. On May 6, WMR reported: "WMR has obtained information from biological researchers that the 1918 Spanish flu genetic sequences were 'manipulated' in order to effect transmission capability. The current H1N1 virus, called 'swine flu,' is reportedly a combination of two forms of human flu, two forms of swine flu (North American and Eurasian), and avian or bird flu . . . Two bio-safety laboratories have been associated with the genetic reverse engineering of not only A-H1N1, the current 'swine flu' strain, but also the deadly Ebola virus. They are the University of Wisconsin-Madison and the National Microbiology Laboratory in Winnipeg, Canada."

WMR has now learned from virus researchers that the current A-H1N1 strain strongly appears tied to vaccinations for the seasonal form on influenza. The hybrid flu began in countries where seasonal vaccinations are commonplace and where A-H1N1 did not respond to the normal seasonal flu vaccination antibody, according to researchers studying the new virus.

What has some researchers alarmed is that the engineers of A-H1N1 purposely planned to make the virus non-responsive to any available vaccine. There is also a suspicion by researchers that the A-H1N1 vaccine under development will trigger a more deadly mutated form of the virus for which the A-H1N1 vaccine will be ineffective.

On May 19, WMR reported: "What researchers have told us is that as long as the current AH1N1 can infect humans, it will not try to mutate. Even though there have been deaths from AH1N1, most of those infected are sick for up to four days, take Tamiflu or similar drugs, and recover with immunity from the hybrid or 'novel' virus . . . However, with vaccinations, the AH1N1 virus will, of course, be rejected by human hosts and cases around the world will decrease. However, then, the virus will begin to mutate in order to successfully infect human hosts. And when that happens, the new, newly-mutated virus will become much more transmissible and more pathogenic. The nightmare scenario is that the new, mutated virus may take on the characteristics of H5N1 or the avian flu. The vaccines administered for AH1N1 will be ineffective against the new strain of H5N1 and the world may face a more deadlier pandemic then the current AH1N1 outbreak. There are scientists at WHO who are aware of this scenario but their alarm has been suppressed by political and economic considerations."

Public health officials in Brazil are now reporting that the A/H1N1 virus is now in the process of mutating, confirming our earlier reports. A new variant of the pandemic virus is showing up in patients in Brazil making treatment more difficult.

On May 13, 2009, WMR reported: "Because of the rapid mutation of the virus and the fact that, unlike 1918, rapid global transportation is now the norm, scientists are predicting that the molecular clock of the A/H1N1 virus, coupled with modern transportation, means that almost all the countries of the world will experience an A/H1N1 outbreak within the next few months."

The prediction about the rate of global infection is being borne out by reports of the virus now being reported in many more nations, including South Africa, Yemen, Qatar, India, and Morocco, as well as uncontained surges in Australia, New Zealand, the UK, Utah, and Argentina.

In another suspicious turn of events, Ivorian national Konan Yao, a former researcher at the Winnipeg laboratory that has been involved in A/H1N1 research and who was arrested by the FBI at the U.S. border crossing on May 5 trying to sneak 22 vials of Ebola and HIV genetic material into the United States for his new job at the National Institutes of Health in Bethesda, Maryland, near Washington, DC, was given his post-plea bargain sentence in federal court in Grand Forks, North Dakota late last month: 17 days in prison which equated to time served and a $500 fine. Yao's federal charge was "failure to present merchandise for inspection," a lesser charge from the original "attempting to bring biological material into the United States without a permit." Yao's new job was at the NIH's Biodefense Research Laboratory. The federal prosecutor who cut the plea deal with Yao is Lynn Jordheim, the Assistant U.S. Attorney in Fargo, who also happens to be the U.S. Attorney's office representative on the Anti-terrorism Advisory Council (ATAC) and Crisis Management Coordinator for the federal jurisdiction and, more intriguing, the "Confidential Human Source Coordinator."

Authorities downplaying the number of those infected with avian flu

WMR has learned from an informed source in the virus research community that little-known U.S. Navy medical groups, known as Naval Medical Research Unit Number 2, headquartered in Jakarta, Indonesia, and Naval Medical Research Group Number 3, headquartered in Cairo, are carrying out research on the artificially-created A/H1N1 human-swine-avian hybrid virus. WMR has also learned that the number of avian flu cases in Indonesia and Egypt are being downplayed by health officials and the international corporate media.

WMR has also learned that the NAMRUs in Jakarta and Cairo have only used local employees to collect avian flu samples from the general population and they are not permitted to conduct research within the laboratories. We have also learned that cases of infections in both Egypt and Indonesia are on the rise but the news is being censored by the Egyptian and Indonesian governments.

During the avian flu outbreak in Indonesia in 2006, the activities of NAMRU 2 were questioned by Indonesian lawmakers. NAMRU personnel have the diplomatic authority to travel anywhere in Indonesia to conduct medical investigations and collect samples. In 2008, Indonesian Health Minister Siti Fadilah Supari paid a surprise facility to the unit in Jakarta. NAMRU 2's operations were suspended temporarily but this past February the Indonesian House of Representatives authorized the renewed operations of NAMRU 2. However, there are suspicions that NAMRU is involved in the obscure area of medical intelligence gathering or "MEDINT" and that much of this intelligence ends up in U.S. biological warfare laboratories in the United States, including Fort Detrick, Maryland.

NAMRU 2 was also accused by Indonesian authorities of taking avian flu and other disease samples from Indonesia and using them to produce vaccines without any compensation or sharing agreement with Indonesia.

NAMRU 2 began in Guam during World War II as a joint operation between the Navy and the Rockefeller Institute. NAMRU 2 then moved to Taipei, Manila, and eventually, Jakarta. NAMRU 2 has detachment units in Laos, Singapore, Thailand, and Cambodia.

WMR has learned the same situation now exists with NAMRU 3 in Egypt. NAMRU 3 is collecting all the avian flu samples in Egypt. NAMRU 3 has a sophisticated laboratory but only Americans work on the research. Egyptians are only authorized to collect samples that are then delivered to a window at NAMRU 3. The same situation is said to exist at NAMRU 2 in Jakarta.

NAMRU 3 has existed in Cairo since World War II. Even during the break in U.S.-Egyptian diplomatic relations after the 1967 Arab-Israeli war, NAMRU 3 remained operational.

On May 13, 2009, WMR reported, "scientists are predicting that the molecular clock of the A/H1N1 virus, coupled with modern transportation, means that almost all the countries of the world will experience an A/H1N1 outbreak within the next few months." According to recent reports, the prediction of scientists about the spread of the A/H1N1 appears to be correct. The virus has now spread to Greece, Slovakia, Estonia, Lebanon, Dominican Republic, Russia, Venezuela, the remote Canadian Arctic territory of Nunavut, Alaska, Romania, Bolivia, Cyprus, Hungary, Uruguay, Taiwan, Paraguay, Honduras, Iceland, Wales, and Ireland.