What Can You Believe About Bird Flu?


Richard Moore

Original source URL:

SIS Press Release 18/05/06
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

A fully referenced version of this article is posted on ISIS members¹ website. 
Details here

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 ³Where¹s the bird flu pandemic?² 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 government¹s chief scientific adviser sir 
David King said the chances of bird flu virus mutating into a form that spreads 
between human are ³very low², and any suggestion that a global flu pandemic in 
humans was inevitable was ³totally misleading² [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

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 they¹ll have to 
protect the food industry.

The chief executive of UK Medical Research Council Colin Blakemore said on BBC 
radio, ³There is no evidence of transmission to people by eating cooked eggs or 
chicken², adding that the only food risk he could see was from ³drinking swans¹ 

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 ³not been implicated in the transmission of the H5N1 avian influenza 
virus to humans.² It stated that, ³humans who have acquired the infection have 
been in direct contact with infected live or dead birds.²

This same EFSA has been criticised recently by the European Commission for ³GMO 
bias² in giving overwhelmingly positive opinions on genetically modified food 
and feed, and often ignoring evidence of hazards (see ³European Food Safety 
Authority Criticised for GMO bias², 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, ³Direct evidence of 
oral infection is lacking, but so too is proof against.²

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 report¹s conclusions [2]. Les
Sims, a consultant for the UN¹s Food and Agriculture Organization (FAO) said 
avian influenza ³has never been and should never have been seen as a food safety
issue.² Bird flu concerns over food ³have a devastating impact on the livelihood
of millions of farmers globally and demonstrate that risk communication on this 
has been a total failure.²

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 can¹t 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 

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 

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 ³Fowl play in bird flu², 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 ³Fowl play in bird flu², 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 ³Where is the 
bird flu pandemic?² this series). Viruses isolated from birds and humans in Kong
Kong in 2003 and 1997 make up clades 1¹ 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 

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, 1¹ 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 ³Fowl play in bird flu², 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.

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