Scott McPherson's Web Presence

The University of Colorado confirms what we always suspected - that the overuse of amantadine in Chinese poultry vaccines has rendered the M2 antiviral essentially useless if H5N1 "goes pandemic."

A brand-new paper from the University of Colorado at Boulder (Go Buffaloes!) has confirmed the resistance of at least 30% of the existing substrains of H5N1 avian flu to amantadine, an M2 antiviral. Further, this study declares that amantadine resistance is now (in laymens terms) part of the natural evolution of the virus, meaning it has become the norm; the standard; the template for virus evolution. Irreversible and permanent, this resistance to amantadine (and also rimantadine) is the direct result of Chinese farmers feeding it to their chickens in a futile effort to beat back H5N1. The presence of amantadine in feed and in vaccines simply hastened the virus's resistance to the antiviral.

Amantadine works against the M2 protein by preventing it from doing its duty; namely, dissolving the outer coating of the virus.  By denying the virus the chance to dissolve its coat, it cannot infect.

Researchers, using among other tools the famed Google Earth API (for Application Programming Interface), have created a template so they can watch in near real-time as viruses, including H5N1, begin to display resistance to certain antivirals and drugs. "Real time" would be defined as the time in which these findings are actually noted, meaning researcher and publication real time, and not time as the real world knows it. Further, real time in this universe is complicated by the lack of shared data, which can render this issue moot if researchers are denied information on drug resistant genetic changes and modifications in the virus itself.

Researchers also speak to the Elephant In The Room, which is Tamiflu resistance. So far, they say, there is no cause for concern. But they hasten to add that it is not yet under the influence of "positive genetic selection," meaning that it H5N1 has not yet settled in to any sort of observable trend toward Tamiflu resistance. Yet.

Of particular interest to us (and probably to Dr. Henry Niman) is the statement that resistance is not being conferred via reassortment, or the mixing of genes as the virus mingles with other copies of itself. Instead, the amantadine resistance is gaining momentum via novel genetic mutations rather than an exchange of RNA segments within cells, according to the author of the study.

Here's the news story:

Bird flu becoming more resistant to antivirals

The avian flu, an Influenza A subtype dubbed H5N1, is evolving a resistance to a group of antiviral drugs known as adamantanes, one of two classes of antiviral drugs used to prevent and treat flu symptoms, said CU-Boulder doctoral student Andrew Hill, lead study author. The rise of resistance to adamantanes -- which include the nonprescription drugs amantadine and rimantadane -- appears to be linked to Chinese farmers adding the drugs to chicken feed as a flu preventative, according to a 2008 paper by researchers from China Agricultural University, said Hill.

In contrast, resistance of the avian flu virus to the second, newer class of antiviral drugs that includes oseltamivir -- a prescription drug marketed under the brand name Tamiflu -- is present, but is not yet prevalent or under positive genetic selection, said Hill of CU-Boulder's ecology and evolutionary biology department. The CU findings should help health administrators around the world plan for the possibility of an avian flu pandemic.

The CU-Boulder study is the first to show H5N1 drug resistance to adamantanes arose through novel genetic mutations rather than an exchange of RNA segments within cells, a process known as re-assortment, said Hill. The research on the mutations, combined with molecular evolution tests and a geographic visualization technique using Google Earth, "provides a framework for analysis of globally distributed data to monitor the evolution of drug resistance," said Hill.

The CU-Boulder-led study appears online in the journal Infection, Genetics and Evolution . Co-authors included CU-Boulder Associate Professor Robert Guralnick, recent CU-Boulder graduate Meredith Wilson, Farhat Habib of Kansas State University and Daniel Janies of Ohio State University.

"As these adamantanes have gotten into nonhuman vectors like birds, the positive selection for resistance to avian flu is rising," said Hill. "If Tamiflu is ever used in the manner of adamantanes, we could conceivably see a similar resistance developing through positive selection."

The research team used an interactive "supermap" using Google Earth technology that portrays the individual gene mutations and spread of the avian flu around the globe, said Guralnick of CU-Boulder's ecology and evolutionary biology department. By projecting genetic and geographic information onto the interactive globe, users can "fly" around the planet to see where resistant H5N1 strains are occurring, said Guralnick, also Hill's doctoral adviser.

For the study, the researchers analyzed 676 whole genomes of Influenza A/H5N1 from National Institutes of Health databases of viruses isolated between 1996 and 2007. The team is comparing how often amino acid sequence changes in genes lead to mutations that affect drug resistance in the H5N1 virus and how often such changes evolve into random mutations that don't affect resistance, Hill said.

The next step is to analyze 2008 data, he said.

First detected in China in 1996, the avian flu has spread throughout Asia and to India, Russia, Pakistan, the Middle East, Africa and Europe by various carriers, including poultry and migratory waterfowl, Hill said. While H5N1 is not highly communicable to humans from birds or between humans, experts are concerned future evolution of this subtype or other subtypes, or genetic re-assortment between subtypes, could make an avian influenza strain more contagious with the potential to cause a pandemic.

"Even if H5N1 is not the flu subtype that develops into the next pandemic, this technique can help us understand the properties of flu viruses and we can use these methods to track mutations in other viruses," said Guralnick. "We can harvest genetic influenza data and monitor it in near real-time, which should give this project some traction to help governments make decisions on managing potential pandemics."

Like the legend of a road map, colors and symbols on the supermap indicate which types of hosts carry the virus or the distribution of genotypes of interest, said Hill. A click by users on viral "isolates" generates computer windows revealing H5N1 mutations linked to positive genetic selection resulting from the spread and use of adamantanes.

http://www.colorado.edu/

Two Zimbabwean peacekeeping soldiers are dead of suspected Ebola infection.

This week's proMED email regarding the spread of Ebola in the Democratic Republic of Congo contained more then the usual bad news. Apparently two members of the African peacekeeping force are dead of Ebola. While the report is unconfirmed, getting the truth out of Congo on Ebola right now is like trying to get a consensus Illinois US Senator seated -- in other words, impossible.

The two dead peacekeeping soldiers were from Zimbabwe, and were assigned to the western Congo region including the province of Western Kasai. The latest Ebola outbreak began there in late November, and the two soldiers were apparently garrisoned within the province. How they contracted the disease is unknown, but since Ebola is a fluid-borne illness (at least so far), it is reasonable to assume they came across infected humans or primates.

And not necessarily living humans or primates. Another report from DR Congo speculates that dead monkeys are harboring the virus and passing it to people.  From China View:

LUANDA, Jan. 6 (Xinhua) -- The dead monkeys found in the forest in the Democratic Republic of Congo (DR Congo) might be behind the outbreak of the Ebola virus in DR Congo's southwestern Kassi province, Angola's official news agency ANGOP reported on Tuesday.

Diosdado Nsue-Micawg, representative of the World Health Organization (WHO) in Angola, was quoted as saying that he feared that the improper handling of the dead monkeys might be the cause of the outbreak of the Ebola pandemic in the DR Congo.

He said although the source of the Ebola virus is so far unknown, it is feared that hunters and women who visit the forest might have been in contact with infected monkeys.

The official also said the WHO has assisted the Angolan government with specific information and instructions to Lunda Norte, Lunda Sul, Moxico, Malanje and Uige provinces that border the DR Congo to revitalize and reorganize the alert and prevention systems.

The WHO representative said the WHO will also help the Angola government with the drafting and implementing of an emergency action plan, the gathering of information on supporting health networks and logistics with a view to effectively handling the possible outbreak of Ebola in the country.

The Ebola virus was first reported in late November last year in DR Congo southwestern province of Kassai, bordering Angola's northwestern Lunda-Norte province.

According to WHO data, three cases of the disease were recorded in the DR Congo and at least 36 suspected cases were recorded, including 12 deaths feared to be related to the disease.

Laboratory tests are now taking place in the DR Congo, Gabon and South Africa.

To prevent the spread of the Ebola pandemic from the DR Congo, Angolan President Jose Eduardo dos Santos on Saturday appointed an ad-hoc commission coordinated by Angolan Prime Minister Antonio Paulo Kassoma.

 It is also not unreasonable to assume that Zimbabwean soldiers might feed themselves, consuming bush meat as they move along the territory.  Whatever the reason, two dead soldiers scares me more than a village full of dead Ebola victims.  Why?  Simply pout, soldiers are more mobile.  They are probably patrolling the countryside, going from village to village, putting down the insurrection or attempting to do the same.  They are, by definition, much more likely to be mobilized and to move via mechanized means such as trucks or halftracks.  And they are likely to be garrisoned in tents, huts or barracks with other soldiers.

To call this situation potentially explosive is to dramatically understate the situation.  Hopefully, tests will show the soldiers died of some other disease, just not Ebola.  But we need to watch this situation very, very closely.  At least as closely as eyes and ears will allow. 

The newswires are absolutely white-hot today over the beath of 19-year-old Beijing woman Huang Yanqing. The Chinese government is reporting that Huang died at 7:20 AM local time yesterday in a Beijing hospital. She was pronounced dead of H5N1 avian influenza.

The case is not so simple. She purchased and ate infected poultry at a local market, just outside the city limits of Beijing, which has not reported avian flu for some time in either poultry or in humans.

Here's the greatest cause for concern: Yanqing had contact with 116 other people (nice of the government to be so precise) and possibly infected a nurse who was attending her.  From Bloomberg, and as reported in the Honolulu Advertiser:

Beijing reports suspected bird-flu fatality

By Stephanie Wong
c.2009 Bloomberg News

Jan. 6 (Bloomberg) — Beijing, the most severely infected city during the 2003 global SARS epidemic, has reported a possible death from avian flu, as an unusually cold winter saps resistance in the Chinese capital.

Huang Yanqing, who died at 7:20 a.m. yesterday in a Beijing hospital, handled the innards of nine ducks bought from a market in Hebei province, which surrounds Beijing, state-owned Xinhua News Agency said today in its English service. She had contact with 116 people, Xinhua said, citing the local health bureau.
The Geneva-based World Health Organization said China’s health ministry informed it today of the death, adding that it is prepared to offer technical assistance, according to a statement sent on PRNewswire.

Health and agricultural authorities culled 377,000 poultry in eastern China’s Jiangsu province in December after finding the H5N1 strain of the bird-flu virus in chickens. Areas where the poultry were raised had been disinfected, other birds were placed under quarantine, while the transport of poultry was restricted.
Contact with migratory birds carrying the virus is one possible cause of infection in poultry. Dead chickens in Hong Kong tested positive for the H5N1 strain last month and India culled more than 250,000 birds in its northeastern region to contain an outbreak.

The H5N1 strain of the avian-flu virus has afflicted 392 people worldwide since 2003, according to the WHO. Almost two of every three cases were fatal.

China has had 31 bird-flu cases in humans and 21 deaths since 2003, according to the WHO. A 24 year-old-man who died in Beijing in 2003 was initially thought to have died from the severe acute respiratory syndrome, or SARS. Subsequent laboratory tests confirmed he had died from the avian flu, making him the first fatality in the Chinese capital from the disease.

Huang, 19, contracted her disease on Christmas Eve and was hospitalized on Dec. 27, according to a statement today on the Beijing health bureau’s Web site.

A nurse recovered from the fever she’d developed after coming in contact with the deceased woman, Xinhua reported.

China’s government was criticized by the WHO for its slow response to the 2003 SARS outbreak, which infected 8,098 people globally, killing 774, almost a third of the cases in the Chinese capital. President Hu Jintao fired health minister Zhang Wenkang and Beijing mayor Meng Xuenong in 2003, after admitting that the city had covered up the number of SARS cases in the city.

An emergency meeting was convened yesterday in Beijing to handle the bird-flu case, Xinhua said without elaborating.

OK, now let's rewind back a few weeks to the revelation that the vaccine used by both the Chinese and the Egyptians has produced a mutant strain of bird flu that has simply mutated/evolved beyond its targets.  Flu does that, duh:  We all know that.  But are we dealing with a new clade, or one of the usual suspects here?

One thing is for sure:  2009 is showing us already that there is much work left for us to do.

 The Indian state of Assam is working overtime to make sure it does not enter the history books as Ground Zero of a bird flu pandemic.

The message boards tracking avian influenza are humming with the news coming out of the Indian state of Assam. As you can see, Assam is located in the eastern part of India, near China, Bangladesh and Myanmar. that area of the world has again been overrun with H5N1 avian influenza.

The response from the Indian government has been formidable. The government has culled hundreds of thousands of poultry. They have rushed in hundreds of animal husbandry workers, and put them all on Tamiflu. They have gone house-to-house, looking for people with fever and upper respiratory infections.

And they have found at least 69 such cases, in both house-to-house and hospital searches. Whether or not these cases are H5N1 has not yet been released. But the Indian government is taking zero chances. And in fact, according to the veteran flu blogger from Italy named Ironorehopper, stockpiles are quite impressive. Ironorehopper reports:

-- Logistics

- 40,000 capsules of Tamiflu, 12,000 surgical masks, 1200 personal protective equipments, 400 N-95 masks, 50 bottles of tamiflu syrup and 8 ventilators have been supplied by MoHFW.
- Sufficient anti-viral drugs and PPE are in stock with the State Government.

In the meantime, West Bengal continues to wrestle with its outbreaks of H5N1 in poultry.  The government in Sikkim has ordered the disinfecting of each and every vehicle that crosses its border with West Bengal, and culling operations everywhere in the nation are intensifying.  This is a serious situation which bears close observation. 

Wisconsin researcher claims another "breakthrough" -- but is he observing protocol with his labwork?

The noted and, to be fair, very capable virus researcher Yoshihiro Kawaoka, has released another research paper regarding the dreaded H1N1 influenza virus and its elusive "smoking gun" of lethality. Kawaoka is affiliated with the University of Wisconsin, which built and named a facility in his name, and with the University of Tokyo.

Researchers unlock secrets of 1918 flu pandemic

http://news.yahoo.com/s/nm/20081229/hl_nm/us_flu1918

WASHINGTON (Reuters) – Researchers have found out what made the 1918 flu pandemic so deadly -- a group of three genes that lets the virus invade the lungs and cause pneumonia.

They mixed samples of the 1918 influenza strain with modern seasonal flu viruses to find the three genes and said their study might help in the development of new flu drugs.

The discovery, published in Tuesday's issue of the Proceedings of the National Academy of Sciences, could also point to mutations that might turn ordinary flu into a dangerous pandemic strain.

Yoshihiro Kawaoka of the University of Wisconsin and colleagues at the Universities of Kobe and Tokyo in Japan used ferrets, which develop flu in ways very similar to humans.

Usually flu causes an upper respiratory infection affecting the nose and throat, as well as so-called systemic illness causing fever, muscle aches and weakness.

But some people become seriously ill and develop pneumonia. Sometimes bacteria cause the pneumonia and sometimes flu does it directly.

During pandemics, such as in 1918, a new and more dangerous flu strain emerges.

"The 1918 influenza pandemic was the most devastating outbreak of infectious disease in human history, accounting for about 50 million deaths worldwide," Kawaoka's team wrote.

It killed 2.5 percent of victims, compared to fewer than 1 percent during most annual flu epidemics. Autopsies showed many of the victims, often otherwise healthy young adults, died of severe pneumonia.

"We wanted to know why the 1918 flu caused severe pneumonia," Kawaoka said in a statement.

They painstakingly substituted single genes from the 1918 virus into modern flu viruses and, one after another, they acted like garden-variety flu, infecting only the upper respiratory tract.

But a complex of three genes helped to make the virus live and reproduce deep in the lungs.

The three genes -- called PA, PB1, and PB2 -- along with a 1918 version of the nucleoprotein or NP gene, made modern seasonal flu kill ferrets in much the same way as the original 1918 flu, Kawaoka's team found.

Most flu experts agree that a pandemic of influenza will almost certainly strike again. No one knows when or what strain it will be but one big suspect now is the H5N1 avian influenza virus.

H5N1 is circulating among poultry in Asia, Europe and parts of Africa. It rarely affects humans but has killed 247 of the 391 people infected since 2003.

A few mutations would make it into a pandemic strain that could kill millions globally within a few months.

Four licensed drugs can fight flu but the viruses regularly mutate into resistant forms -- just as bacteria evolve into forms that evade antibiotics.

Kawaoka has been fixated on the H1N1 Spanish Flu virus (and with Ebola) for awhile now, and press releases have followed Dr. Kawaoka with regularity since 2004. Any Google search with the following criteria "Kawaoka 1918 flu" will net you an impressive list of headlines.

Kawaoka's work has included a 2007 study in a Level 4 biolab in Canada where he infected apes with the 1918 pandemic virus; and this latest study, where he spliced the 1918 virus with current flu viruses and infected ferrets with various hybrid pandemic/seasonal variants until he came up with a few cocktails that induced severe and often fatal reactions in the ferrets.

Of concern to some is the fact that he is messing with gene splicing to begin with, thereby creating new flu variants using the 1918 virus. Recall that in September, 2007, Kawaoka was slapped hard for his playing fast and loose with the Ebola virus. In fact, as reported by the AP on September 20, 2007, the National Institutes for Health (NIH) actually suspended Kawaoka's work with Ebola due to inferior lab conditions.

Study of Ebola virus in U.S. lab halted

Facilities at Wisconsin university were not secure, NIH says

http://www.msnbc.msn.com/id/20892122/

MADISON, Wis. - University of Wisconsin-Madison research on the deadly Ebola virus was conducted for a year in a less-secure laboratory than required, until the National Institutes of Health alerted the school to the problem.

The deadly virus itself was never present in the laboratory, said Jan Klein, UW-Madison biological safety officer. Instead, DNA copies of the virus were being studied to better understand one of the world's most dangerous pathogens.

Klein said no one was ever at risk, though an infectious virus could have been produced if the research material had been combined with other components. "But that was not part of any planned experiment and would not be done by accident," she said.

The research was conducted there from 2005 until being halted in October 2006. Klein characterized the problem as a technical violation rather than a safety violation.

"NIH took a broader read of the guidelines than we were aware of and we were using," she said.

The researcher, Yoshi Kawaoka, a professor of virology in the School of Veterinary Medicine, said he immediately moved the research to a Canadian lab with higher security after the NIH said the UW-Madison laboratory was not secure enough for the research.

"We see this as a difference in interpretation" with the NIH, he said in an e-mail Thursday.

NIH spokesman Don Ralbovsky said he was looking into the matter and had no immediate comment.

Kawaoka is a leading researcher on infectious diseases such as bird flu and Ebola. The university retained him last year by promising to build a $9 million research institute after he received a lucrative offer elsewhere. (bold mine)

The university approved Kawaoka's study initially for a Biosafety Level 3, Klein said. Several of UW-Madison's laboratories are Level 3 labs, but none are Level 4, where the most stringent guidelines to contain the most dangerous pathogens are applied.

Klein said Kawaoka was pressing to conduct the research in a less restrictive Level 2 lab. When the university asked the NIH for guidance, it learned the material was restricted to a Level 4 lab.

I can best describe what Kawaoka was doing as working with a "fax" of the Ebola virus. But the point is that protocol was not observed, and that is why the NIH took the extreme steps of shutting down Dr. Kawaoka's research. He then moved the work to Canada, ostensibly to gain access to a level 4 lab, but to also perhaps extricate himself from the prying eyes of now-awake federal regulators.

It was this same Canadian lab which produced Kawaoka's last headline:

Study uncovers a lethal secret of 1918 influenza virus

Jan. 17, 2007

http://www.news.wisc.edu/13360

The study "proves the 1918 virus was indeed different from all of the other flu viruses we know of," says Kawaoka, a professor in the UW-Madison School of Veterinary Medicine and at the University of Tokyo.

The new study, conducted at the Public Health Agency of Canada's National Microbiology Laboratory in Winnipeg, Manitoba, utilized the 1918 flu virus, which has been reconstructed by researchers using genes obtained from the tissues of victims of the great pandemic in a reverse genetics process that enables scientists to make fully functioning viruses.

Upon infection, the virus grew rapidly in the infected animals, suggesting the agent somehow sets the stage for virulent infection. "Somehow, early in infection, this virus does something to the host that allows it to grow really well," says Kawaoka. "But we don't know what that is." (bold mine)

In the new study, conducted in a high-level biosafety laboratory (BSL 4) at the Public Health Agency of Canada's National Microbiology Laboratory, seven primates were infected with the reconstructed 1918 virus. Clinical signs of disease were apparent within 24 hours of infection, and within eight days, euthanization was necessary. The rapid course of the disease mirrors how quickly the disease ran its course in its human victims in 1918.

In addition to Kawaoka, authors of the new Nature paper include Darwyn Kobasa, Steven M. Jones, Hideki Ebihara, Friederike Feldman, Judie B. Alimonti, Lisa Fernando, Yan Li and Heinz Feldman of Canada's National Microbiology Laboratory; Kyoko Shinya of Japan's Tottori University; John C. Kash and Michael G. Katze of the University of Washington; John Copps of the Canadian Food Inspection Agency's National Centre for Foreign Animal Disease; and Yasuko Hatta, Jin Hyun Kim, Peter Halfmann and Masato Hatta of UW-Madison.

The new study was supported by the Public Health Agency of Canada, the Japanese Ministries of Education, Culture, Sports, Science and Technology, and private grants to Kawaoka.

But wait! Didn't Kawaoka figure out what "it" was back in 2004? Yet another breathless headline, this time from Science Daily:

Gene From 1918 Virus Proves Key To Virulent Influenza

http://www.sciencedaily.com/releases/2004/10/041007081335.htm

ScienceDaily (Oct. 7, 2004) — MADISON - Using a gene resurrected from the virus that caused the 1918 Spanish influenza pandemic, recorded history's most lethal outbreak of infectious disease, scientists have found that a single gene may have been responsible for the devastating virulence of the virus.

Writing today (Oct. 7, 2004) in the journal Nature, virologist Yoshihiro Kawaoka of the University of Wisconsin-Madison and the University of Tokyo, describes experiments in which engineered viruses were made more potent by the addition of a single gene. The work is evidence that a slight genetic tweak is all that is required to transform mild strains of the flu virus into forms far more pathogenic and, possibly, more transmissible.

The results of the new work promise to help scientists understand why the 1918 pandemic, a worldwide outbreak of influenza that killed 20 million people, spread so quickly and killed so efficiently, says Kawaoka, who has studied influenza viruses for 20 years. The finding also lends insight into the ease with which animal forms of the virus, particularly avian influenza, can shift hosts with potentially catastrophic results.

"Replacing only one gene is sufficient to make the virus more pathogenic," says Kawaoka, a professor of pathobiological sciences at the UW-Madison School of Veterinary Medicine. In the Nature paper, Kawaoka and his colleagues describe how a Spanish flu gene that codes for a key protein changed a relatively benign strain of flu virus from a nuisance to a highly virulent form.

In the late 1990s, scientists were able to extract a handful of genes from the 1918 virus by looking in the preserved lung tissue of some of the pandemic's victims. Subsequently, the genes were sequenced, including two critical genes that make hemagglutinin and neuraminidase, the protein keys that help the virus enter and infect cells.

Using a comparatively mild form of influenza A virus as a template, Kawaoka's team added the two 1918 genes that code for hemagglutinin and neuraminidase and infected mice with the engineered viruses.

"Here we demonstrate that the [hemagglutinin] of the 1918 virus confers enhanced pathogenicity in mice to recent human viruses that are otherwise non-pathogenic in this host," Kawaoka and his colleagues write in the Nature report. Moreover, the viruses with the 1918 hemagglutinin gene caused symptoms in the mice - infection of the entire lung, inflammation and severe hemorrhaging - eerily similar to those exhibited by human victims of the 1918 pandemic.

Scientists and historians have long speculated about why the 1918 Spanish flu virus was so virulent. Theories range from lack of modern medical care and antibiotics, which had not yet been developed, to the already weakened state of many victims due to war and the tumultuous social conditions of the time.

"There also were people who thought the virus was different in terms of its virulence," Kawaoka says. The results of the new study tend to support the idea that the virus was inherently more dangerous.

Another important result of the new study is that it supports the idea that the 1918 Spanish flu virus was avian in origin, but already adapted to proliferate in humans. That insight is important as scientists and public health officials view birds as a primary reservoir of influenza A virus, strains of which can sometimes jump species to infect other animals, including humans.

According to Kawaoka, it's known that avian strains of the virus have slightly different receptors - key proteins on the surface of the virus that act like a key to unlock and infect host cells - from those on flu viruses that infect humans.

"That restricts transmission from avian species (to humans) to some extent, but not completely," Kawaoka notes.

The receptors on the virus with the gene from the 1918 virus, Kawaoka says, readily recognized their complements on human cells. "That tells you that there was a change in receptor recognition after introduction from avian species to humans. It recognized the human receptor even though it came from an avian species. That's why it transmitted so efficiently among humans."

A third and intriguing finding of the study is that blood from the now very elderly survivors of the 1918 pandemic had high antibody titers to the engineered virus, Kawaoka says.

"People who were infected with this virus in 1918 still have high antibodies, even after 80 years," he says.

That scientifically interesting finding, Kawaoka explains, suggests that another outbreak of flu like the 1918 pandemic would spare many very old people who had had a brush with the virus more than 80 years ago. The irony in that, according to Kawaoka, is that influenza often extracts its heaviest toll on the elderly.

I used to read scientific papers voraciously -- that is, until I had to start paying for them to gain access. I am sure Dr. Kawaoka is doing some really fine research up there in Madison. But I cannot help but feel I am reading the same headline over and over and over and over again. Kawaoka claims that he found that "single gene" back in 2004 when he spliced 1918 genes onto common seasonal influenza A. Then he said in 2007 that he didn't know what "it" was. Then in December 2008, he says he has found "it" again! And this time, "it" is three genes.

And forgive me, I cannot help but feel that somehow, grant dollars are tied to these headlines.  "Publish or perish" is the mantra when it comes to these types of careers.  But can someone tell me in terms I can understand what the difference is between these three studies?  I am reminded of Omar Bradley's comment that giving Patton a headline meant he was good for another twenty miles.  Now substitute the word "grant" for "miles."

Also let me ask the question no one else seems to be asking:   What assurances are there, given Dr. Kawaoka's apparent belief that he knows better than the authorities what level of biosecurity is proper for these experiments, that someone with a kill switch is looking over his shoulder? 

Dr. Robert Webster has stated publicly that he believes the 1977 "age-specific pandemic" (my words) of H1N1 was the result of a Soviet lab accident.  Wouldn't it be terribly ironic if a hybrid pandemic virus was foisted upon society by those looking to solve its lethality who moved their ops to another nation because they perhaps didn't like who was peering over their shoulder?