Sunday, January 01, 2012

5th estate obtains University of Texas prelim report on "accidental" H5N1 lab release

Taking no chances now by releasing H5N1 at multiple points around world trying to avoid pinpointing origin of virus; preliminary lab incident report at bottom

By Pamela Drew

The story of the mysterious, dead birds in Austin was proclaimed solved by the Associated Press today. That's simply not true, actually nothing could be farther from the truth. A potentially deadly accident occurred and the parties responsible for public safety are busy covering up the event. Thanks to being in the loop on a research network, the updates are coming to me via e-mail. It seems almost like BREAKING NEWS; we are at the leading edge of the story, even if, it's not leading by much.

On January 12, The Sunshine Project released details of the accident at the University with the following in the report:
According UT records obtained by the Sunshine Project, the accident happened on a Wednesday afternoon, 12 April 2006. A postdoc was working in the Molecular Biology Building ("MBB") on the University of Texas campus in Austin, just a couple minutes' walk away from tightly packed dormitories, the kind of place where a virulent new influenza strain might eagerly take hold. A little over a kilometer south is the Texas Capitol and a warren of state office buildings teeming with public employees.
Centrifuge Accident Aerosolizes Genetically Engineered Influenza
The postdoc was working alone in a beefed-up BSL-3 laboratory wearing a full lab suit. A respirator system provided oxygen through an air hose. The high-tech safety measures were in place because the viruses in the lab were not your average flu. They were something much more dangerous. They were genetically engineered influenza strains that mixed and matched genes of the common human H3N2 influenza and those of deadly H5N1 "Bird Flu". The kind of unpredictable reassorted flu strain that public health officials fear could cause the next human pandemic.
BSL-3 Lab
 Keep in mind the people supplying the information are not political bloggers or conspiracy theorists. They are research scientists working with deadly pathogens. They are not prone to panic, or alarmists claims like a well meaning, ill informed group of tree huggers. Nothing against all my tree hugging buddies out there, but these folks aren't like us. They understand far better than most of us will in a lifetime, the risks they deal with and what constitutes cause for concern. They are worried and the University is stonewalling. An open letter and list of questions was sent to the University. They are pasted below and I will keep an eye out for updates and anything leaking from News beyond Newsvine. Links are below.

19 January 2007

An Open Letter to the University of Texas at Austin

Dr. Juan M. Sanchez
Vice President for Research
University of Texas at Austin
P.O. Box 7996, Main Building 302
Austin, TX 78712-1111
By fax (512-471-2827) and e-mail (

Members of the Institutional Biosafety
Committee of the University Of Texas at Austin

Dear Dr. Sanchez and IBC Members:
Laboratory accidents involving highly pathogenic influenza pose a
grave public health risk. On 12 April 2006, the University of Texas
at Austin experienced an incident involving genetically engineered
H5N1 influenza ("Bird Flu") at UT's Molecular Biology Building

Since 12 September 2006, the Sunshine Project has sought to ascertain
details of this incident. Unfortunately, the University of Texas at
Austin has resisted a full public accounting and has produced
inconsistent and fragmented accounts of what occurred. Some of the
University's recent statements to members of the news media directly
contradict the information contained in UT's own documents released
under freedom of information laws.

The Sunshine Project has drafted ten questions for the University
regarding the incident. In the interest of public health and public
accountability, we request that you please promptly answer them.

If you have questions, please don't hesitate to contact me.

Edward Hammond
Ten Questions for the University of Texas at Austin
Concerning the H5N1 Laboratory Incident of 12 April 2006
1) Recently, UT has stated that the virus only contained one gene
from H5N1 and has specified that this gene was a non-structural gene.
Yet the UT accident report refers to "some genes" from H5N1, and the
minutes of the UT Institutional Biosafety Committee specifically
state that "The virus had H5N1 structural proteins included". Please
explain these discrepancies and provide the genetic composition of
the virus involved in the accident.

2) If the University is confident that no leak occurred, why was the
researcher placed on Tamiflu and continued to take Tamiflu for a
week, and;

3) why did the University decontaminate the entire lab "as if the
contamination had occurred"?

4) The University states that it is confident that prior infection
with H3N2 influenza would immunize against the virus used in the lab.
Was the researcher vaccinated against the H3N2 strain before
initiating the work? If not, why not?

5) The UT accident report states "University reseachers DO NOT work
with H5N1. Our researchers work with non-contagious elements of that
virus." Why was the University handling these "non-contagious
elements" of H5N1 at BSL-3?

6) Neither the accident report, nor the IBC minutes, nor the
University's recent statements to reporters are factually consistent.
Why is the University failing to produce a consistent set of facts
and description of this incident?

7) With the sole exception of the IBC minutes, which must be released
under federal guidelines, why did the University petition the
Attorney General for permission to keep every single one of its
records about this incident a secret?

8) Why did the University not report this incident to the National
Institutes of Health, whose Guidelines require (Section IV-B-2-b-(7))
that accidents be reported?

9) What specific facts contained in the University of Texas accident
report released to the Sunshine Project does the University of Texas
now claim are incorrect? Please specifically and clearly enumerate

10) If the University's accident report is seriously flawed, why did
the University release the report with no indication that it contains

 Any opinions expressed here are those of the author and do not necessarily reflect those of The 5th Estate.

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Kobe University Report of Academic Workshop on Influenza - “Preparing for the Next Influenza Outbreak”

The Publisher, 5th Estate was the English editor for this report

Report of Academic Workshop on Influenza

“Preparing for the Next Influenza Outbreak”

1) Date:  26 March 2010

2) Venue:  Lecture Room, School of Medicine, Kobe University

3) Language:  English

4) Objectives:  We are now entering the new millennium where both weaponized and “novel” infectious diseases are being experimented with by many world governments and universities.  As these diseases now threaten the lives and health of people on a scale never before imagined, it is essential to create and implement protocols to respond promptly and appropriately to these threats.  Therefore, in order to realize a relatively safe and anxiety-free society it is also necessary to build a protective system from a global perspective, to counter infectious diseases which spread with lightning speed as modes of transportation become ever faster and travel by citizens of the world increases exponentially every 

This workshop, “Preparing for the Next Influenza Outbreak,” is organized to present a venue allowing researchers from the EU Member States and Japan to exchange their experiences and useful information.  This information may then be shared with colleagues and health care professionals from a broader range as we prepare for the next pandemic.

5) Program: 

13:10 -13:40 “Experience of pandemic (H1N1)2009 outbreak in Kobe”.

Dr. Michio HAYASHI, Director, Division of Infectious Diseases and
Division of Respiratory Medicine, Division of Infection control and
Prevention, Kobe City Hospital Organization Kobe City Medical Center
General Hospital

Chair: Dr. Kentaro IWATA, Professor, Division of Infectious Disease
Therapeutics, Center for Infectious Disease (CID), Kobe University

13:40 - 14:25 “2009 Influenza Pandemic”

Prof. Yoshihiro KAWAOKA, Director, International Research Center
for Infectious Diseases and Division of Virology, Department of
Microbiology and Immunology, Institute of Medical Science,
University of Tokyo

Chair: Dr. Yoshitake HAYASHI, Professor, Division of Infectious
Disease Pathology, Center for Infectious Diseases (CID), Kobe

14:25 - 15:10 “Determinants of Virulence of Zoonotic and Pandemic Influenza Viruses"

Prof. Dr. Ron FOUCHIER, Professor in Molecular Virology at the
Department of Virology, Erasmus Medical Center Rotterdam

Chair: Dr. Hak HOTTA, Professor, Division of Microbiology, Centre
for Infectious Diseases (CID), Kobe University 

15:30 - 16:15 “Clinical Aspects of Pandemic Influenza H1N1 2009”

Dr. Norio SUGAYA, Director, Department of Pediatrics, Keiyu Hospital
Chair: Dr. Soichi Arakawa, ICD, Infection Control Team, Kobe
University Hospital 

 16:15 - 17:00 “Adaptation Mechanisms of Influenza A Viruses”

Dr. Kyoko SHINYA, Associate Professor, Division of Zoonosis,
Graduate School of Medicine, Kobe University

Chair: Dr. Takaaki NAKAYA, Associate Professor, International
Research Center for Infectious Diseases, Research Institute for
Microbial Diseases, Osaka University 

17:00 - 17:45 “Novel Influenza Virus-Specific Polymerase Inhibitors”

Dr. Martin Schwemmle, Professor of Virology at the Department of
Virology, University of Freiburg

Chair: Dr. Yasuko MORI, Professor, Division of Clinical Virology,
Center for Infectious Diseases (CID), Kobe University

Coordinator: Prof. Akiko MAKINO, Research Associate, Division of
Zoonotic Virology, Center for Infectious Diseases (CID), Kobe
5) Results:

         Dr. Michio Hayashi, during the session of “Experience pandemic (2009) in Kobe” disclosed the strategy taken in controlling influenza pandemic of 2009 in Kobe City Hospital, Kobe, Japan.  The first outbreak of pandemic 2009 flu in Kobe was confirmed on May 15 when seven people were confirmed to have been infected.  Since then the rate of infection rose steadily and reached its peak on May 21 with 446 confirmed cases for the entire city.

         Responding to the outbreak of pandemic flu, immediate action and countermeasures were taken.  The major efforts by Kobe city were the establishment of isolation units for outpatient with fever or “Hatsu Netsu Gairai” in several hospitals such as Kobe City Hospital; the set up a 24-hour hotline center for fever consultation.  Outpatient and fever isolation units were built as emergency external installations outside the hospital, along with a considerable bio-security level facility.  Samples from patients with fever were examined with real time PCR, and any positive result would be subjected to a second test for confirmation.

         Kobe city hotline center for fever consultation provided information for citizens about the things related to pandemic 2009 flu infection.  Most of the questions were “what should I do when I catch fever?”  The peak of these calls was reached on May 19 with a number of 2,678 callers.  Approximately 20% of the callers were calling from their homes. 

         These prevention and control actions during 2009 influenza pandemic in Kobe demonstrated the preparedness of the Kobe city government in facing the possibly incoming pandemic. 

         Dr. Yoshihiro Kawaoka, at the second session titled “2009 Influenza Pandemic” spoke about important knowledge of the novel H1N1 2009 influenza virus.  The virus was first identified to have infected people in Mexico at the end of March 2009, and has since been rapidly circulating worldwide.  This condition had urged the World Health Organization (WHO) to raise the world pandemic alert to level four.  This had been the first world pandemic for over 40 years.

         The cause of the disease pandemic flu 2009 is a new influenza A virus subtype H1N1.  The virus was rapidly circulating among the human population all over the world and caused relatively mild illness.  Of all cases, 1 to 10% of the patients were hospitalized.  The susceptible age novel H1N1 2009 infection was different compared to the 2007-2008 flu season infection.  The most susceptible ages of novel H1N1 2009 ranged from 24 to 40 years old, meanwhile the 2007-2008 flu tended to infect babies (around 0-4 years old) and elders (over 80 years old).  Mortality was mostly caused by secondary bacterial infection, and also in people with risk factors such as pregnancy and young age.  Among children, mortality was mostly identified around the ages 5 to 9 years for novel H1N1 2009 infection, and 0 to 4 years old for 2007-2008 seasonal flu infection.

         Phylogenetic study of novel H1N1 2009 revealed that the virus consisted of the genes from a re-assortant swine flu virus (combination of classic swine, North America avian and H3N2 human flu type) and Eurasia avian-like swine flu virus.  Receptor analysis showed that the virus had preference to both human-type and avian-type receptors even though the human-type receptor was most determined.

         A pathogenicity testing of novel H1N1 2009 flu compared to seasonal flu virus had showed that novel H1N1 2009 flu was able to cause severe inflammation in most lobes of the deep lung, whereas seasonal flu infection mostly showed only partial mild changes in the deep lung.

         Currently, the control and treatment of pandemic 2009 flu infection relies on a neuraminidase inhibitor known as oseltamivir or Tamiflu, since the virus found having resistance to M2 blockers such as adamantenes.  However, to anticipate the development of oseltamivir resistant pandemic 2009 flu strains, further research is needed to find alternative drugs while preparing for the next pandemic.  Other compounds such as T705 and CS-8959 had been evaluated and seemed to be promising as the next anti influenza drugs.

         Dr. Ron Fouchier at the third session, “Determinants of Virulence of Zoonotic and Pandemic Influenza Viruses" describes the virulence markers of influenza virus and circumstances of 2009 pandemic in the Netherlands.  Based on its pathogenicity, avian influenza (AI) is divided into highly pathogenics (HPAI), for example H5 and H7 subtypes, and low pathogenic (LPAI) strains. HPAI H5N1 had decimated poultry industries and caused human casualties in many countries, while the H7N7 subtypes had also proved to have been transmitted to humans.

         The most distinctive virulence marker is found in the cleavage site of the HA gene, where the site will be recognized and cleaved by certain protease to promote replication. Cleavage of HPAI has a pattern of multiple basic amino acids, RERKKR, which is cleavable by multi proteases, while LPAI has a pattern of PQIETR that is cleavable only by protease trypsin-like protease limited in human upper respiratory tract.  However, studies showed that a LPAI strain might have increased its pathogenicity when multiple basic amino acids were experimentally introduced into its HA cleavage site.

         In 2003, an outbreak of AI H7N7 subtype had been reported in the Netherlands.  The virus infected 255 farms that caused approximately 31 million birds to be culled. A total of  89 H7N7 human infections were reported.  Human cases showed conjunctivitis, and one was reported to have died.  Amino acid sequence from the outbreak showed amino acid changes from glutamic acid (E) to lysine (K) in PB2 segment, or also called E627K. Further study showed this amino acid substitution related to high pathogenicity of the virus in infected mice.  This substitution had also been previously known as one of the virulence markers in the H5N1 virus.

         In the case of novel H1N1 2009 flu, the virus had characteristics of being able to reach lower airways faster, replicate faster and reach higher titer.  These findings suggest that the virus has reached complete adaptation.  Sequence analysis of novel H1N1 2009 flu fatal cases from the Netherlands showed amino acid mutation of the HA segment at position 222 from aspartic acid (D) to glycine (G), which has been studied as well as one of the HA receptor binding sites.  Furthermore, this amino acid mutation was also found in Ukraine and Norway fatal cases.

         Further study in mice and ferrets showed that virus having HA D222G did not show any remarkable virulence change when compared to wild virus.  However, a receptor binding experiment showed that HA D22G showed binding preference to 2-3 alpha sialic acid which is commonly found in the colons of birds and the human deep lung. 

         Dr. Norio SUGAYA at the session titled “Clinical Aspects of Pandemic Influenza H1N1 2009” spoke about the success of Japan in limiting the mortality of pandemic flu in 2009. 

         The influenza pandemic has caused millions of deaths in most countries, including Japan.  Records mention that during the “Spanish flu” pandemic in 1918, Japan suffered a 0.87% death rate, about 0.45% during 1957-58 pandemic and about 0.076% during 1968-1970 pandemic.  In the 2009 pandemic, about 1-2% of patients were hospitalized and 0.1-0.2% patients died globally.  Of the total world death, 0.001% was reported from Japan, or in other words, equal to one death in Japan per 10,000 deaths globally.  Compared to influenza season 2008 which caused 272 deaths, the pandemic influenza H1N1 2009 caused relatively fewer deaths, with 186 deaths.  Based on these facts, Japan is ranked as the country with the lowest mortality rate caused by H1N1 2009 in the world.  The contributing factors of the mortality rate of H1N1 2009 pandemic flu infection are pregnancy, secondary infection, accompanying disease and young age.

         WHO recommendation for H1N1 2009 virus drugs are Tamiflu (per oral) and Peramivir (intra-vein).  During the 2009 pandemic in Japan, doctors prescribed Tamiflu for patients according to the WHO guidelines even though WHO guidelines for the antiviral drug mentions that only patient-at-risk groups should be treated with antiviral drugs. Tamiflu is a commercial name of oseltamivir phosphate, a neuraminidase inhibitor.  It works by blocking the site of enzymatic activity of neuraminidase, so that the virus loses the ability to replicate further.  In Japan, Tamiflu has been the main prescription for seasonal flu long before and it was used in pandemic H1N1 2009 influenza patients.  Dosage recommendation for treatment is 75 mg twice a day for 5 days, while dosage for prophylaxis is 75 mg per day for a week after possible exposure.  The use of Tamiflu during the 2009 pandemic in Japan seemed to not only have suppressed the number of deaths among patients, but also saved the life of patients-at-risk, as a pregnant woman had survived after being treated with Tamiflu. 

         Dr. Kyoko Shinya at the session titled “Adaptation Mechanism of Influenza Virus” presented the results of her studies of influenza A receptors in human airways and ostrich involvement in the selection H5N1 avian influenza virus.

         Avian influenza or bird flu virus H5N1 subtype had infected over 100 people worldwide.  Most of the cases had a contact history with birds, and human to human transmission was relatively rare.  Sialic acid with sugar linkage has been known as the influenza virus host receptor.  Human type receptors consist of sialic acid with 2-6 alpha sugar linkage, meanwhile the bird type receptor consists of sialic acid with 2-3 alpha sugar linkage.  Dr Shinya studied the type of sialic acid in human airways epithelial cells and found that human upper and lower airways had different types of sialic acid.  Human upper airways were found to have sialic acid 2-3 sugar linkage or human type receptors, but lower airways from the branch of bronchus to alveolus sialic acid were dominated with 2-3 sugar linkage or avian type receptors.  This finding explained why avian influenza virus airborne transmission is relatively limited among humans.  However, when an eventual transmission from bird to human occurred, it might reach human deeper lung and efficient viral replication would occur.

         Amino acid at position 627 in the influenza A virus PB2 segment has been known to affect the temperature sensitivity of the virus.  Virus with lysine at PB2 627 (PB2-627Lys) has been known to have efficiently replicated in the upper respiratory organs in mice.  From the Influenza Virus Resource Database, it was found that PB2-627Lys appeared in isolates from Ratitae birds (e.g. ostrich, emu, rhea) in high prevalence.  When placed in ostrich and chicken embryo fibroblast, the H5N1 virus developed PB2-627Lys mutation in ostrich lines after six passages, unlike when it was passed in the chicken line.  Infection experiments with the ostrich chicks with the H5N1 virus in the absence of  PB2-627Lys, showed that PB2-627Lys developed in the virus, isolated from several organs of the ostrich chicks. 

         Dr Martin Schwemmle at the session of “Novel Influenza Virus-Specific Polymerase Inhibitor” spoke about polymerase inhibitors as future anti-influenza drugs.

         Knowledge of influenza replication cycle has become the basis for anti-influenza drugs.  Known anti-influenza drugs have a neuraminidase inhibitor mode of action along with M2 channel blockers and polymerase inhibitors.  Consequently, the future target for new drug development such as cap-binding inhibitors, endonuclease activity etc. may be promising. 

         The correct assembly of three viral polymerase subunits PB1, PB2 and PA is required for viral RNA synthesis and infectivity.  Influenza A PA had been studied to bind with N-terminus PB1 at a small binding location with 1-25 amino acid residues.  Polymerases are mostly conserved among influenza viruses, however some different amino acids are found at the PB1 binding sites of different viral sub-types.  The initial study was done by using small fluorescence peptide (Green Fluorescence Protein/GFP) to mimic a peptide which is intended to bind to the PB1 binding location that interrupted the formation of polymerase complex.  This experiment was proven to inhibit the polymerase activity of the influenza A and B viruses. 

         Because several amino acids are present in the PB1 binding site, further experimentation is needed to find out which amino acid, and which location will produce the maximum virus inhibition effect.  After locating the suitable peptide, the screening of compounds specifically blocking PA-PB1 interaction and inhibiting growth of influenza A and B virus may be promising for the discovery new anti influenza drugs.
6)  Conclusions

         The characteristics of influenza viruses are different among subtypes.  Adaptation of influenza viruses in certain host cells reflect mutations that change the virus characteristics and finally resulted as a species-barrier leap.  The influenza pandemic of 2009 was caused by the influenza A virus subtype H1N1 which is a re-assortment of human, swine and bird flu segments.  The causes relatively mild disease but spreads very quickly among human populations. 

         Currently available antiviral drugs such as oseltamivir and peramivir are still effective for the current 2009 pandemic, however consecutive research in antiviral drugs is still ongoing while anticipating the next pandemic.  Polymerase inhibitors are one of the effective anti influenza drugs.  The PB1-binding domain is small and unique peptide as a site where PA binds and activates the polymerase complex.  A single amino acid change in the PB1-binding domain alters the pathogenicity of the virus.  Therefore, compounds which target PB1 binding sites can be isolated for the next anti-influenza drugs.

         Japan has experienced influenza pandemic since the 1918 “Spanish flu,” until the 2009 H1N1 flu.  For the current 2009 influenza pandemic, Japan follows WHO guidelines for influenza control and treatment, and one of those is the use of oseltamivir (Tamiflu) for treatment and prevention.  Tamiflu recommended usage is 75 mg Tamiflu twice a day for six days for treatment, or 75 mg per day for seven days after exposure for prevention. Using this guideline, Japan has suppressed the number of pandemic flu deaths in the country, and also recorded the lowest death rate globally.

         Local and regional governments in Japan attempted several control measures during the pandemic flu 2009.  Kobe city, for example has succeeded in constructing an outpatient ward with the fever isolation unit/”Hatsu Netsu Gairai” to triage, give first aid action for incoming patients with fever, and a hotline center for fever consultation.  Current experience should be applied as one of the strategies to combat the next pandemic. 

COMING IN A FEW HOURS : Medical advisory : Novel H5N1: Precautions, prophylaxis, treatments; next installment H5N1 virologist smoking gun e-mails

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some files

Friday, 15 May, 2009 20:24
This sender is DomainKeys verified
"Ida - Teridah Ernala" <>
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Message contains attachments
epiflu_sequence update may 07 2009.fasta (663KB), Sw_H1_nj.tre.pdf (242KB), Sw_M_01May09_annot.trees.pdf (170KB), Sw_M_nj.tre.pdf (250KB), Sw_N1_nj.tre.pdf (231KB), Sw_NP_nj.tre.pdf (249KB), Sw_NS_nj.tre.pdf (245KB), Sw_PA_nj.tre.pdf (144KB), Sw_PB1_nj.tre.pdf (143KB), Sw_PB2_nj.tre.pdf (144KB)
Hi Robert,
Here I send you some files. I don't think they will help much.
The files are phylogenic tree of all genes of swine flu, and sequence data updated 7 May (there is newer version but I havent't download it). Again you will need software to open the sequences. It takes time though.
Have a nice weekend.


 More on Kobe
Monday, 18 May, 2009 13:51
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The virus has hit over than 100 people in Kobe until now, in just three days. I'm fine, and no one really showed severe symptoms anyway.
But this is very strange thing because mostly students are affected without any history of travelling abroad.
If this is keep continuing, the WHO will level up the pandemic threat to level 6. And they're now thinking to produce vaccine.
I have bad feeling about vaccine Robert. I assume when vaccination is started, the second deadly wave will come. Maybe new H1N1 or reassortant of H5N1 and H1N1 or H5N1 itself.
Naturally, as long as virus can infect human, it won't try to mutate. It's better just let the virus to infect, get fever for 3-4 days, taking tamiflu and others, then recovers. When it happens, the virus has been defeated and we get immunity.
By vaccination, virus will be rejected. Maybe the world will see the cases decrease, and everyone's happy.
But it won't take long. Instead of giving up, virus will be keep on circulating and try to find a way to infect effectively. This may cause massive mutation of virus, to be more transmissible and more pathogenic.
I'm talking in nature's way.

In the other hands. Think about this. If this virus is really spread intentionally by some parties, please think as if you were in their shoes:
1.You spread virus, a highly transmissible one but with mild sickness.
2.People are panic, and forgetting other thing that is really threatening human kinds. The H5N1.
3.What do you expect from people? Of course you will assume (and everyone assumes) that people will try to make vaccine. That's your objective isn't it?
4.When you created the virus, you knew very well about the gene. So you knew already what kind of vaccine people will try to establish. The vaccine that may stop the outbreak for a while, but triggering a deadly second wave. The H5N1.

Robert, if this is really spread intentionally, someone who responsible must have tought far forward.

I'm getting insane.


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Re: rough analysis

Wednesday, 15 July, 2009 15:07
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"Southeast Asia News" <>
What I know, this company has fooled Indonesians.
They came with their vaccine, telling it was swine flu vaccine. My people were so naive to believe them and buying their vaccine. But unfortunately it wasn't.

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Re: rough analysis

Thursday, 16 July, 2009 07:54
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"Southeast Asia News" <>

I don't know anyone there, unfortunately. Well forget it, don't get bothered. 
This company just pissed me off. How come they did that!! Meanwhile now they're producing the real vaccine but only for European countries.
I will write about this, just a short comment.




The real truth on 9/11 slowly continues to bleed out

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The Geopolitics Of The United States, Part 1: The Inevitable Empire

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