Despite gains from threat of bird flu, pandemic preparedness is patchy ... With the World Health Organization discussing whether to declare, as Nature went to press, that a swine influenza pandemic has arrived, doctors, scientists and government officials say the enormous preparedness efforts of recent years have aided the world's response to the virus. "Clearly, the global preparedness for dealing with an influenza outbreak is much better now than it was five or six years ago," says virologist Malik Peiris of the University of Hong Kong. But there have been some hiccups, due largely to the mismatch between the pandemic scenarios envisaged and the one that has arrived. Most nations had prepared for a pandemic sparked by the deadly A(H5N1) avian influenza virus, which kills up to 60% of those infected, but the A(H1N1) swine flu virus epidemic has been much less severe so far. "Many nations built their plans around the idea that a pandemic strain would evolve in southeast Asia, that we would recognize it early, and that we would be able to contain it," says Eric Toner, a physician and preparedness analyst with the University of Pittsburgh Medical Center's Center for Biosecurity in Pennsylvania. "None of that turned out to be true."

After decades of warnings about the inevitability of another pandemic of influenza, it is astonishing that health officials have failed to make clear to the public, even to many colleagues, what they mean by the word pandemic. Generations of people have used the term to describe widespread epidemics of influenza, cholera and other diseases. But as the new H1N1 swine influenza virus spreads from continent to continent, it is clear that a useful definition is far more complicated and elusive than officials had thought. And what is at stake is far more than an exercise in semantics. A clear understanding of the term is central to the World Health Organization’s six-level staging system for declaring a pandemic, which in turn informs countries when to set their control efforts in motion. Dictionaries and medical journals offer little guidance. Their definitions can be too vague or too narrow, contradictory and clouded by jargon. “There is a lot of misinformation in the medical literature, and it is really quite hard to figure out what is and what is not a pandemic,” said Dr. David M. Morens, an epidemiologist at the National Institute of Allergy and Infectious Diseases who has been studying the history of pandemics. The word implies the rapid spread of an infectious disease to many countries in different regions, hitting each with more or less the same severity. But in fact, severity varies — not all people are infected at the same time, and not every country need be affected. And there can be many other factors, including the numbers and percentages of people falling ill and dying; a population’s vulnerability to the disease, based on previous rates of infection; and the quality of health care facilities and disease monitoring systems. Not least is that scientists do not know precisely how pandemics arise, what fuels them, why they vary in their lethality, why some occur in waves and why they stop.

This work supports our findings with the H5N1/H1N1 data regarding early hyper-induction of interferon-related and other innate immune genes in the response to H5N1.

Six years of worrying about bird flu did much to prepare the United States for the current swine flu outbreak, federal officials and an independent monitoring group said Thursday, but they cautioned that there were still gaps in planning. After the H5N1 avian flu emerged widely in Asia in 2003, killing about 60 percent of those infected by it, many countries took steps to head off the crisis that would emerge if that virus were to acquire the ability to jump easily from human to human. It has not, but a number of the measures were helpful. These are some of them: ¶The federal government stockpiled 50 million courses of Tamiflu. ¶New vaccine factories were opened. ¶Pandemic plans were written, and emergency drills were held.

The Ministry of Health of Egypt has reported a new confirmed human case of avian influenza A/H5N1 on 01 June 2009. The case is a 4-year old female child from the Kefr El Sheikh District of Kefr El Sheikh Governorate. Her symptoms started on 30 May 2009 with fever, cough and sore throat. She was admitted to Kefr El Sheikh Fever Hospital on 31 May 2009. The patient received oseltamivir and is in a stable condition.

The Ministry of Health of Egypt has reported two new confirmed human cases of avian influenza on 26 May 2009. The two cases are from two separate districts of Sharkia Governorate. The first case is a 4-year old male from Hehia City, Hehia District. His symptoms began with fever on 24 May 2009. The second case is a 4-year old female from Abo Hammad District. Her symptoms began with fever on 23 May 2009. Both cases were admitted to Zagazig Fever Hospital where they received oseltamivir and are in a stable condition. Investigations into the source of infection indicated that the above two cases had close contact with dead and sick poultry.

Bowing to pressure, the World Health Organization announced Friday that it would rewrite its rules for alerting the world to new diseases, meaning the swine flu circling the globe will probably never be declared a full-fledged pandemic. Dr. Keiji Fukuda, the deputy director general making the W.H.O. announcement, said that he could not predict exactly what the new rules would be but that criteria would include a “substantial risk of harm to people,” not just the geographic spread of a relatively benign virus. The six-point system was created in 2005 when the threat was H5N1 avian flu, which has a fatality rate of about 60 percent. But the system does not take into account a virus’s lethality, and in the current outbreak, some countries have complained that the warning system created panic and pressure for border closings, even though the strain was less deadly.

Avian influenza viruses do not thrive in humans because the temperature inside a person's nose is too low, according to research published today in the journal PLoS Pathogens. The authors of the study, from Imperial College London and the University of North Carolina, say this may be one of the reasons why bird flu viruses do not cause pandemics in humans easily. There are 16 subtypes of avian influenza and some can mutate into forms that can infect humans, by swapping proteins on their surface with proteins from human influenza viruses. Today's study shows that normal avian influenza viruses do not spread extensively in cells at 32 degrees Celsius, the temperature inside the human nose. The researchers say this is probably because the viruses usually infect the guts of birds, which are warmer, at 40 degrees Celsius. This means that avian flu viruses that have not mutated are less likely to infect people, because the first site of infection in humans is usually the nose. If a normal avian flu virus infected a human nose, the virus would not be able to grow and spread between cells, so it would be less likely to damage cells and cause respiratory illness. The researchers also found that when they created a mutated human influenza virus by adding a protein from the surface of an avian influenza virus, this mutated virus struggled to thrive at 32 degrees Celsius. This suggests that if a new human influenza strain evolved by adopting proteins from an avian influenza virus, this would need to undergo further changes in order to adapt to the conditions in the human body. The researchers reached their conclusions by growing cells from the human airway and infecting them with different human and avian influenza viruses, including H5N1, to see how well the viruses grew and spread. The human influenza viruses grew equally well in the cells whether they were maintained at 37 degrees Celsius, our core body temperature, or at 32 degrees Celsius, the temperature of the nose. In contrast, the four avian influenza viruses tested grew well at 37 degrees Celsius but grew very slowly at 32 degrees Celsius. When the researchers added proteins from an avian influenza virus to a human influenza virus, the human influenza virus also grew slowly and struggled to replicate at 32 degrees Celsius.

Influenza type A viruses are endemic in aquatic birds but can cross the species barrier to infect the human respiratory tract. While transmission from birds to humans is rare, the introduction of novel avian influenza viruses into immunologically naïve human populations has significant pandemic potential. Avian influenza viruses are adapted for growth at 40°C, the temperature of the avian enteric tract. However, the human proximal airways, the likely site of initial inoculation by influenza viruses, are maintained at a cooler temperature (32°C), suggesting that zoonotic transmission may be limited by temperature differences between the two hosts. Using an in vitro model of human ciliated airway epithelium, we show that avian influenza viruses grow well at 37°C, a temperature reflective of distal airways, but are restricted for infection at 32°C. A panel of genetically manipulated human influenza viruses possessing avian or avian-like surface glycoproteins were also restricted at 32°C, but not 37°C, suggesting that avian virus glycoproteins are not adapted for efficient infection at the temperature of the proximal airways. Thus, avian influenza virus infection is restricted in the human proximal airways due to the cooler temperature of this region, thus limiting the likelihood of zoonotic and subsequent human-to-human transmission of these viruses.