Science in Society Archive

What Can You Believe About Bird Flu?

Dr. Mae-Wan Ho looks behind the propaganda and expert pronouncements that frighten you and give false reassurance in turn

Is the bird flu pandemic imminent?

Anyone following the streamers of headlines on bird flu in the popular media will be thoroughly bewildered. Experts and politicians have been telling us that a bird flu pandemic is bound to happen; all it takes is for the deadly H5N1 Asian strain of bird flu that kills more than half of its human victims to mutate so it can pass from human to human instead of from infected chickens to humans. That could happen at any time; a state of emergency is declared, and drugs and vaccines are being stockpiled around the world; all to the benefit of the pharmaceutical industry (see “Where’s the bird flu pandemic?” this series).

The arrival of a dead swan in Fife Scotland at the beginning of April 2006 that tested positive for H5N1 was met with due alarm. Bird flu is spreading to Britain, and the pandemic is surely just around the corner.

A week later, however, the British government’s chief scientific adviser sir David King said the chances of bird flu virus mutating into a form that spreads between human are “very low”, and any suggestion that a global flu pandemic in humans was inevitable was “totally misleading” [1].

Anyway, no more wild birds have tested positive, and that seemed to have given false reassurance to those who believe bird flu is transmitted by wild migrating birds.

Bird flu is not a food safety issue?

There has been little mention that infected meat and other poultry products could bring the dreaded virus to our supermarket shelves and farms. But people know that anyway. Sales of poultry products have plummeted so much that the EU has already announced payments to compensate the industry.

The pundits have been out in force giving reassurances that the pandemic is not going to happen after all, despite the alarm raised previously, which has already delivered great profits to the drug industry, so now they’ll have to protect the food industry.

The chief executive of UK Medical Research Council Colin Blakemore said on BBC radio, “There is no evidence of transmission to people by eating cooked eggs or chicken”, adding that the only food risk he could see was from “drinking swans’ blood”.

A journalist in Nature reporting on the debate among scientists commented that Blakemore and others have downplayed the risk of catching bird flu from eating chickens and eggs, for fear of damaging public confidence and the poultry industry [2].

The European Food Safety Authority (EFSA) published a prominent scientific risk assessment paper in March 2006, advising that poultry products are safe to eat and have “not been implicated in the transmission of the H5N1 avian influenza virus to humans.” It stated that, “humans who have acquired the infection have been in direct contact with infected live or dead birds.”

This same EFSA has been criticised recently by the European Commission for “GMO bias” in giving overwhelmingly positive opinions on genetically modified food and feed, and often ignoring evidence of hazards (see “European Food Safety Authority Criticised for GMO bias”, this issue).

Many scientists disagree with the opinion of the EFSA on bird flu, as they have on GMOs. There simply is insufficient evidence to say that eating infected poultry would not transmit the virus. As Masato Tashiro, a virologist at the National Institutes of Infectious Diseases in Tokyo said, “Direct evidence of oral infection is lacking, but so too is proof against.”

Furthermore, there is no guarantee that people would always cook the products sufficiently well, or take hygienic precautions while preparing food to prevent uncooked meat contaminating other food items that are eaten raw.

Albert Osterhaus, a virologist at the Eramus Medical Centre in Rotterdam, said available evidence suggests that the gastro-intestinal tract in humans is a portal of entry for H5N1. He was part of a team of scientists that showed cats became infected with H5N1 after being fed infected chickens. They exposed cats to H5N1 virus by three different routes: intrathecally (injection into the fluid surrounding the brain and spinal cord), feeding on infected chickens, or close contact with respiratory-infected cats. They found that regardless of the route of exposure, the virus replicated in the respiratory tract as well as in other tissues of the cats; and infected tissues contained the viral antigens wherever there is severe necrosis (tissue death) or inflammation. Inflammation association with H5N1 infection was found in the nerve tissue of the gut wall only in cats that had eaten virus-infected chickens, suggesting a new portal of entry for influenza viruses in mammals [3].

All of the cats excreted virus through the respiratory tract as well as the digestive tract. In humans, shedding of the virus in the faeces has been observed, and therefore the possibility of faecal-oral transmission should be taken into account.

An EFSA spokesperson said the agency stands by the report’s conclusions [2]. Les Sims, a consultant for the UN’s Food and Agriculture Organization (FAO) said avian influenza “has never been and should never have been seen as a food safety issue.” Bird flu concerns over food “have a devastating impact on the livelihood of millions of farmers globally and demonstrate that risk communication on this has been a total failure.”

But Jody Lanard, a physician and risk-communication consultant based in Princeton, New Jersey, USA, disagreed. She said such advice shows little has been learnt about risk communication since the British agriculture minister publicly fed his young daughter a hamburger at the height of the BSE (bovine spongiform encephalitis) crisis.

The pundits can’t be trusted

A 2005 European Commission poll showed that almost half of European citizens believe the authorities favour economic interests over consumer health, and they no longer believe what the regulators say. In many cases, they believe just the opposite of what the regulators tell them, which is why the poultry industry is suffering.

As for the fear that the Asian bird flu will damage the industry, the first outbreak of bird flu was reported in Norfolk Britain 27 April 2006. Some 35 000 birds had to be culled. The dreaded H5N1 was not the culprit, but another, H7 strain [4], later identified to be H7N3 [5], which does not cause serious disease in humans, but Japan has promptly slapped a ban on imports of UK poultry.

This outbreak highlights the fact that bird flu is already endemic in commercial farms in Europe as it is in the United States. Officials from the Department of the Environment, Food and Rural Affairs admitted that an H7 strain of avian flu was last detected in Britain in 1987 [4], and outbreaks of H7 avian flu have since occurred throughout the world. In 2003, 31 million birds had to be culled in the Netherlands after an outbreak of the H7N7 strain of bird flu. In 2002, H7N7 broke out on poultry farms in Virginia USA, and 4 million turkeys and chickens were slaughtered. The only comfort is that H7 infections in humans are mild, and only one vet working on the outbreak in the Netherlands died after developing pneumonia.

The outbreak is also a grim reminder that factory farms are the breeding grounds, reservoirs and incubators of bird flu viruses, not wild migrating birds or backyard farms (see “Fowl play in bird flu”, this series)!

Is it safe to eat poultry products?

The existing evidence does suggest that eating infected poultry runs the risk of contracting the virus, as the cat feeding study shows. Not only can cats catch the virus by eating infected dead birds, they can then pass it on to other cats [6]; there is also unconfirmed evidence of human to human transmission, according to a report from the World Health Organization (WHO) Global Influenza Program Surveillance Network [7]. A cat was found with the H5N1 virus on the German Baltic island of Rügen near where 100 birds have died from the H5N1 virus [6, 8], which confirms the laboratory findings.

Furthermore, back in October 2004, 147 tigers out of 441 died or were killed after some of them become infected with H5N1 from eating raw chicken carcases; subsequent investigation found that at least some tiger-to-tiger transmission of the virus had occurred [8].

Thus, eating meat and eggs that are not sufficiently cooked is definitely not a good idea, especially if you do not know where the meat and eggs have come from.

Now is the time to buy locally from organic free-range farms, which may need all our support lest they become victims of politically motivated propaganda.

The genetic evidence

Influenza A viruses, of which H5N1 is a member, cause diseases in many other species including humans, pigs, horses, mink, cats, and marine animals. They have a genome that comes in 8 segments of RNA, and apart from the usual mutations and recombinations of which viruses are prone, different strains of influenza A viruses can exchange segments (a process referred to as re-assortment). This makes it easy, at least in principle, to create a new deadly virus that causes epidemics (see “Fowl play in bird flu”, this series).

H5N1 first emerged in Hong Kong in 1997, where it caused the deaths of 6 of 18 infected persons [9]. The virus was believed eradicated by the slaughter of all poultry in Hong Kong, but new types of H5N1 continued to emerge in poultry in Hong Kong in 2000 and 2001; and in 2003, antigenically and biologically novel H5N1 killed one of two infected humans.

The World Health Organization Global Influenza Program Surveillance Network analysed the genomes of H5N1 viruses taken from birds and humans in Asia [7] and showed that all the genes in the viruses are of avian influenza origin. So reassortment of genome segments between human and bird influenza A viruses was not involved in the current epidemic, as in earlier ones.

Of the three influenza pandemics in the last century, the 1957 H2N2 and 1968 H3N2 pandemic viruses were avian-human reassortments in which three and two of the eight avian gene segments respectively got into an already circulating human-adapted virus. The origin of the genes of the 1918 influenza virus H1N1, estimated to have killed about 50 million worldwide, is still unknown [10].

Researchers found that the H5N1 viruses separate out into two clades (distinct genetic lineages) with non-overlapping geographic distributions. Viruses isolated from the Indochina peninsula form a tight cluster within clade 1, whereas those from several surrounding countries - China, Indonesia, Japan and South Korea – form a more divergent (less tightly clustered) clade 2. Clade 1 viruses were isolated from both humans and birds in Vietnam, Thailand and Cambodia, but only from birds in Laos and Malaysia. They are resistant to the adamantine drugs but sensitive to neuraminidase inhibitors (see “Where is the bird flu pandemic?” this series). Viruses isolated from birds and humans in Kong Kong in 2003 and 1997 make up clades 1’ and 3 respectively.

Most H5N1 isolated from humans are antigenically homogeneous and distinct from avian viruses circulating before the end of 2003. Some viruses isolated in 2005 show antigenic drift (genetic mutation), but the HA genes from viruses isolated from humans are nevertheless closely related to the HA from H5N1 viruses of avian origin, retaining the specificity for bird-type cell surface receptor, and differing from the nearest gene in bird isolates of the same year in 2-14 nucleotides.

These findings are consistent with the epidemiologic data that suggest humans acquired their infections by direct or indirect contact with poultry or poultry products. Both clades of H5N1 from the 2004-5 outbreak have a multiple basic amino acid motif at the cleavage site, which is a defining feature of highly pathogenic avian influenza viruses. Among all H5N1 isolated collected in east Asia since 1997, only those in clades 1, 1’ and 3 appear to be associated with fatal human infections.

Taken together, the results indicate that the H5N1 viruses from human infections and the closely related avian viruses isolated in 2004 and 2005 belong to a single genotype, often referred to as genotype Z, and can be traced back to viruses isolated in 1997 in Hong Kong and from geese in China.

Thus, viruses from the 1997 H5N1 epidemic may have been circulating in Asia since without causing any reported human infections until the two confirmed cases in Hong Kong in February 2003. Where and how have they been circulating?

Intensive poultry farming & bird flu

In an earlier study, researchers found that H5N1 influenza viruses were isolated from apparently healthy domestic ducks in Mainland China from 1999 to 2002; and these viruses were becoming progressively more pathogenic for mammals as time passed [9].

Twenty-one viruses isolated were confirmed to be H5N1 subtype, and antigenically similar to the virus that was the source of the 1997 Hong Kong bird flu haemagglutinin gene, and all were highly pathogenic in chickens (most causing 100% mortality, although the earliest isolates were less lethal). The viruses were increasingly pathogenic for mice the later they were isolated. The earliest seven isolates were non-pathogenic or of low pathogenicity, the next seven of relatively more pathogenic, and the last four highly pathogenic. All pathogenic viruses replicated in the lung.

The genetic findings suggest that H5N1 had been circulating among domestic fowl in Asia since the 1997 epidemic in Hong Kong. And while circulating in domestic ducks, H5N1 viruses gradually acquired the characteristics that make them lethal in mammals including humans. One possible explanation is the transmission of duck H5N1 viruses to humans, the selective evolution of the viruses in humans, and their subsequent transmission back to ducks.

Thus, commercial factory farming could be the reservoir, breeding ground and incubator for deadly epidemic viruses like H5N1, as consistent with other evidence (see “Fowl play in bird flu”, this series).

How likely is the bird flu pandemic?

Many experts are saying that the only barrier between a pandemic of bird flu among birds and one among humans is if the H5N1 mutates its HA gene to recognize the human-type cell surface marker rather than the bird type.

As it turned out, human cells deep in the lower respiratory tract do have the bird-type receptor, which is why the virus can enter those cells and cause severe pneumonia; although the progeny virus is less easy to pass on than if, like human influenza viruses, it could enter and replicate in the cells of the upper respiratory tract as well [11]. Is that the only barrier that keeps away the bird flu pandemic?

Things are not that simple, according to the team of researchers in Erasmus Medical Center in Rotterdam, the Netherlands. Left to its own devices, successful species jumps in nature are relatively rare. That is because complex adaptations are needed for a virus to get established in a new species and transmit from host to host within that species [12]. These complex adaptations including genetic differences constitute biological barriers between species, which can only be breached by genetic modification. That is why genetic modification is dangerous, as I, and others have been warning since genetic engineering began. The SARS virus of the last pandemic did breach species barriers and was highly infectious as it passed from one human host to numerous others, it made many more people ill and caused many more deaths. There is indeed evidence that extensive genetic engineering of corona viruses may have been contributed to creating the SARS virus [13, 14].

What are the barriers preventing a virus to get into a new host [12]?

First of all, there are barriers to prevent the virus from entering the body, such as mucus, alveolar macrophages, and epithelium (linings of organs and tissues). There are specific receptors governing the entry into cells. The HA on the viral coats of the avian influenza viruses preferentially bind to carbohydrate chains attached to the receptor protein ending in a sialic acid in a-2,3 linkage to a galactose, whereas the HA on human influenza viruses prefer an a-2,6 linkage. The lower respiratory tract cells in humans have carbohydrate chains on receptors ending in SA-a-2,3-gal, however, which is why fatal pneumonia can occur in humans infected with the virus.

Once within the cell, the virus must replicate. Many avian influenza viruses can infect mouse cells but not replicate; often because the viral polymerase differs between avian and mammalian influenza viruses in residue 627 of the polymerase protein PB2, which is usually glutamic acid in avian viruses and lysine in mammalian viruses. So this might be another barrier. In experimentally infected mice, a glutamic acid to lysine mutation at this position in the PB2 protein of H5N1 virus results in increased virulence and in the ability of the virus to invade organs other than the lungs. Both H5N1 virus from human patients in Asia and H7N7 virus from a fatal human case in the Netherlands possess a lysine at this site. Lysine is also in the PB2 in H5N1 viruses isolated from the thousands of dead wild water-fowl in mid-2005 from Qinghai Lake in China.

The replicated virus must be released from the host cell to infect more cells or be shed from the host. In influenza, progeny virus particles are bound to host cell receptor carbohydrate chains by their haemagglutinin. Viral neuraminidase cleaves these carbohydrate chains, thus releasing the newly produced virus from the cell surface. Like the respective haemagglutinins, neuraminidases from avian influenza viruses have a preference for the SA-a-2,3-gal-terminated chains, whereas those from many human influenza viruses prefer the a-2,6 linkage.

Even if progeny virus exits one host cell, host innate immune responses may hinder the infection of other cells. Interferons may induce uninfected cells to enter an antiviral state that inhibits viral replication. The viral NS1 polypeptide acts as an antagonist to interferon induction in infected cells by sequestering double-stranded RNAs or suppressing host post-transcriptional processing of mRNAs. NS1 also may help the virus to replicate in interferon-treated cultured cells.

In order to spread from the respiratory tract to other susceptible tissues, the virus needs to enter the lymph and/or blood system, and be successfully transported to other tissues. In poultry, whether infection is localised or systemic depends on the amino acid sequence at the cleavage site of HA. The cleavage is required for the haemagglutinin to become fully functional. Low pathogenic influenza viruses require extracellular proteases that are limited to the respiratory and gastrointestinal tracts to cleave the precursor haemagglutinin, whereas highly pathogenic avian influenza viruses have changes in the cleavage site that allow the precursor HA to be processed by ubiquitous intracellular proteases, resulting in fatal systemic infection. The HAs of H5N1 viruses all have this change, which is a motif of basic amino acids.

From their sites of replication, viruses need to be transmitted to new hosts. Dissemination of progeny viruses form the infected host occurs through shedding in respiratory, enteric, or urogenital secretions. Human influenza viruses replicate mainly in the upper respiratory tract and are usually readily transmitted via droplets formed during coughing or sneezing. By contrast, H5N1 virus typically infects human cells in the lower respiratory tract and so may be less easily shed from the infected patient.

Finally, it is well established in epidemiology theory that, as the proportion of susceptible hosts in the population, s, drops (as individuals become infected, then recover, or die), the number of secondary cases per infection, R, also drops, R = sR0. If R<1, as is currently the case for H5N1, an infection will not cause a major epidemic. But if R is even modestly greater than one, a novel infection may spread locally, with potential for further spread in the absence of control.

For novel infections that jump species, there is no pre-existing specific immunity. (Although as many others have pointed out, boosting our natural innate immunity through good nutrition will give us the best protections yet against any new disease agent.) Pre-existing immune protection can sometimes reduce the number of susceptible hosts, and hence R. For instance, humans who had previously encountered an influenza virus with the N2 neuraminidase may have been partially protected in the 1968 H3N2 pandemic that followed the global circulation of H2N2 viruses. In addition, cross-reactive T cells (which kill virus-infected cells) also may contribute to immunity against other subtypes of influenza viruses.

Influenza is difficult to control because a long infectious period coincide with a period of transmission before symptoms become apparent and quarantine measures can be taken; as opposed to SARS, in which the transmission period coincides with the appearance of symptoms.

Faulty replication of RNA viruses within an individual can generate mutants that by chance have the capability of being transmitted. This was highlighted in January 2006 when samples from a patient infected with H5N1 virus in Turkey was found to have a mixed population of viruses, some of which expressed haemagglutinin with an amino acid sequence associated with an increased affinity for SA-a-2.6-Gal.


It would be foolish to be complacent about eating infected poultry products. On the other hand, the bird flu pandemic is not just around the corner, though it could happen if we do not address the real cause of bird flu: the ever-expanding intensive poultry farming and the globalised food trade.

All the evidence summarised in this and other articles in the series points to intensive poultry farming as the reservoir and incubator for deadly bird flu viruses, while the globalised trade in live birds and poultry products are the main routes of disease transmission.


  1. “Risk of human flu outbreak ‘low’”, BBC News, 9 April 2006,
  2. “Bird-flu experts question advice on eating poultry With H5N1 in wild birds, is it safe to eat chicken and eggs?” Declan Butler, published online. 10 April 2006,
  3. Hampton T. Avian flu researchers make strides Medical News & Perspectives. JAMA 2006 (March 8), 295, 1107-8.
  4. “35,000 birds to be culled in new avian flu outbreak”, Ian Sample, The Guardian, 27 April 2006.
  5. “Japan bans UK poultry as bird flu cases spread”, Alok Jha, The Guardian, 1 May 2006
  6. “Cat dies of bird flu in Germany”, Debora MacKenzie, news service, 28 February 2006,
  7. The World Health Organization Global Influenza Program Surveillance Network. Evolution of H5N1 avian influenza viruses in Asia. Emerging Infectious Diseases 2005, 11, 1515-21
  8.  “Bird flu virus kill a domestic cat in Germany”, Actualites News Environment, 1 March 2006,
  9. Chen H, Deng G, Tian G, Li Y, Jiao P, Zhang L, Liu Z, Webster RG and Yu K. The evolution of H5N1 influenza viruses in ducks in southern China. PNAS 2004, 101, 10452-7.
  10. Stevens J, Blixt O, Tumpey TM, Taubenberger JK, Paulson JC and Wilson IA. Structure and receptor specificity of the hemagglutinin from an H5N1 influenza virus. Science 2006, 312, 404-10.
  11. “Cell barrier shows why bird flu not so easily spread among humans”, University of Wisconsin Press Release, 22 March 2006,
  12. Kuiken T, Holmes ED, McCauley J, Rimmelzwaan GF, Williams CS, Grenfell BT. Host species barriers to influenza virus infections. Science 2006, 312, 394-7.
  13. Ho MW and Cummins J. SARS and genetic engineering? Science in Society 2003, 18, 10-11.
  14. Ho MW. SARS virus genetically engineered? Science in Society 2003, 19, 36-37.

Article first published 18/05/06

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