What Can You Believe About Bird Flu?

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What Can You Believe About Bird Flu?

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Thu, 18 May 2006 15:52:40 +0100

 

 

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ISIS 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

members' website. http://www.i-sis.org.uk/full/WCYBABFFull.php

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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? "

http://www.i-sis.org.uk/WTBFP.php 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 " ,

http://www.i-sis.org.uk/EFSACRGMOB.php 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 " ,

http://www.i-sis.org.uk/Fowl-Play-in-Bird-Flu.php 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.

 

Conclusion

 

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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