Avian (Bird) Flu
Dr Jamie Love
8 October 2005 ©
8 October 2005 ©
About eight years ago I wrote the article below ("Chicken Flu" - recombinant genes on the loose!) to explain the flu; the disease, the virus and its genetics. I have left the article unchanged and in its entirety because it is still relevant and acts as a good history of what has gone on in this news-worthy area. It describes the first cases of avian flu, also know as H5N1, which occured in 1997.
However, due to a flood of emailed questions I decided to include this "preamble" to provide some updates, answers and anticipate your concerns.
Where is it?
As far as I know (mid-October 2005) the avian flu epidemic (H5N1) has been confined to Asia where it has infected many birds. Over 100 million birds have been killed but most were killed by their keepers, trying to control the epidemic, instead of the virus itself. However, it would be wrong to think the H5N1 is harmless to birds - it's a bird killer!
Europeans are getting worried because the avian flu is moving westward (through Russia) carried by flocks of waterfowl. UPDATE - 13th October 2005 - Some birds in Turkey (the country) have been confirmed to have H5N1 (and suspected in Romania).
How bad is it?
There have been slightly more than a hundred confirmed cases of H5N1 infection in people causing about 60 deaths - a 50% death rate! 
All these cases are in Asia (Vietnam, Thailand, Cambodia and Indonesia but many experts feel that China could be hiding its avian flu deaths because China has a "reputation" for doing this). Most of the human cases have been linked directly to contact with poultry infected with H5N1.
There have been a few cases of what appears to be human-to-human transmission but this is not clear. Even among those cases the spread did not (has not) continued beyond one person. That's a good sign that these particular cases are either not true human-to-human transmission or that this strain of H5N1 is not terribly contagious.
Is there a vaccine?
No, not for H5N1. Researchers are working on an H5N1 vaccine but don't expect it this year (flu season).
There is no reason to believe that the "normal" flu vaccine(s) will protect against H5N1 - but the elderly, etc. should still get their annual flu shot/jab to protect against "normal" flu.
Is there a drug for treatment?
Sort of. The current strain of H5N1 (killing birds and some people in Asia) is resistant to two antiviral medications commonly used to fight flu - amantadine and rimantadine. To other antiviral medications, oseltanamavir (Tamiflu) and zanamavir, have not been tested but might work. All these drugs are by prescription only and must be monitored by a physician. (And, no, I cannot give you a prescription nor do I have any of these drugs.)
Should I kill my pet chickens, parrot, etc?
NO! You don't have to worry about getting avian flu from your birds. The worry, in general, is that a bird flu will jump into a human but that jump is a rare event - thus not to be feared. That's a mutation and produces "patient one". However, once that event occurs, the spread from human to human is to be feared! That's the epidemic. Only one person need be infected by the bird flu for it to take hold (the mutation and shift to a new species) and that is much more likely to occur in Asia and on a poultry farm (where there's a high density of sickly birds tended by people who are more likely to make contact) not among pets.
You are more likely to die of a tetanus infection from a chicken's scratch or lung problems from the bird "poo" or asthma from its feathers than from your pet's flu.
By the way, cooking kills the flu virus so even infected poultry is safe if cooked properly. Of course, you should always cook birds properly before eating them anyway!
How can I avoid the avian flu?
Don't visit chicken farms or markets in Asian! 
So far, the only confirmed cases have been in Asia and among folks who handle lots of chickens.
What if it becomes a human-to-human epidemic?!
At that point stop worrying about birds and start worrying about people! 
IF (that's a big "IF") it becomes a human epidemic, you should do whatever you can to avoid the flu. Keep out of crowds (total isolation would be best but is impractical) and away from sneezes.
How long does the virus last (on door knobs)?
The flu virus (particle) is easily destroyed. Sunlight, especially the UV part, and dry air will render the particles non-infectious. (And, of course soap will too.)
How long it takes to "kill" the virus depends upon the specifics. An hour or two should kill most flu viruses on door knobs (for example). But it's hard to say. These kinds of things are a statistical progression, known as a bell-shaped curve, so there are always a little left over after many hours.
Is this hype or is there reason for concern?
Let's put some perspective on this.
Generally speaking, a "killer flu" epidemic occurs every few decades. Some are worse than others. The most recent flu epidemic occurred in 1968 and wasn't too bad. The most deadly flu in recent history killed over 20 million people in 1918 and it was very similar to the H5N1 that we are concerned about now.
Today, we have much better medicines and healthcare (at least in the developed nations) but we also have much more global travel which helps flu to spread. Some experts have been quoted as saying that the next killer flu epidemic could kill more than 100 million! Maybe they're right - or maybe "100 million" is more likely to get quoted by every newspaper on the planet while "10 to 100 million" just isn't so exciting.
Here's a headline that you missed - "Two million people die each year from tuberculosis (TB)". That's each year! Spread that out over several decades (the time between killer flu epidemics) and that's a large number of deaths. But TB is, for the most part, ignored by folks who are all worked up about bird flu. Many TB victims are in underdeveloped countries - another reason TB is ignored. Besides, most TB is easily cured with simple antibiotics (found in developed nations). However, multi-drug resistant TB (MDR-TB) is on the increase and very hard to treat. MDR-TB is now found in more than 4% of new TB cases in Eastern Europe, Latin America, Africa and Asia. As the World Health Organization puts it "Given the increasing trend towards globalisation, trans-national migration, and tourism, all countries are potential targets for outbreaks of MDR-TB." (I won't discuss this further but you can google "multi-drug resistant tuberculosis" to learn more.)
My opinion? At this time (mid-October 2005) I have a feeling of deja vu. Read the article below (written in 1998) and you might get the same feeling.
Should I panic?
No, not yet. 
But now would be a good time to learn more about viruses and flu so please enjoy my (old) article below.
25 January 1998 ©
The media have discovered what many scientists have known all
along - viruses are amazing and scary. Unfortunately, the media are more concerned with scaring you than educating you, so you're
wise to have found Science Explained.
(Here we'll do both!)
Mankind has always been under the threat of a new, more dangerous
virus emerging and causing massive epidemics. Our modern transportation
systems make it all the easier for such a virus to spread quickly
throughout the world. Man's constant exploration and encroachment
in previously inaccessible parts of the world make it more likely
that something nasty might emerge. However, it is worth noting
that viruses have always been with us, evolving ways to reproduce
and spread. Viruses, like humans, are just playing the evolution
game.
But VIRUSES CHEAT!
What exactly is a virus?
| A virus is a bit of genetic material packaged in a protective coat. The genetic material may be DNA or RNA depending on the type of virus. The protective coat is called a capsid. Not only does it protect the delicate nucleic acid inside, but the capsid also helps the virus infect host cells. Some viruses have an additional outer envelope of proteins, sugars and lipids stolen from the host cell in which it has been made. The complete virus "particle" - nucleic acid, capsid and envelope (if it has one) - is called a virion. |
Virus classification is based upon characteristics of the three
parts of the virion. It is a complex system that requires detailed
knowledge about nucleic acid types and structures, virion shapes,
binding of specific antibodies (this has to do with immunity), and
may even include the nucleic acid sequence itself!
The group names of
viruses are not easy to follow because they're often in Latin
and named after a type of disease which only
one member of that group causes. For example, the family of Herpesviruses
includes not only the virus that causes herpes (herpes simplex),
but also the virus that causes chicken pox and shingles (varicella-zoster),
and another virus that causes mononucleosis and some cancers (Epstein-Barr
virus). Another example of this confusion is that the viruses
which cause hemorrhagic fever (a very deadly disease) are found
in three different families (Arenaviruses, Filoviruses
and Arboviruses). It's no wonder that student doctors have
so much difficulty learning them all. Don't worry about the details
but be aware that viruses with similar names, or that cause similar
diseases, may or may not be similar viruses.
Where do viruses come from? Where do they get their genes?
The origin of viruses is poorly understood, but most virologists (people who study viruses) agree that each virus got started by copying a few useful genes from their host cells. Viruses are ignorant of any patent or copyright laws, they just make a copy of what they find useful in the host's genome and move on. Often that useful gene is intimately involved in the host's reproduction, food gathering, cell communication or other essential function of the cell. Over the generations viruses mutate their stolen genes and when a particularly useful mutation comes along, the virus will use it to further its own survival, usually to the detriment of its host. As the years and generations go by these viruses can even switch over to other species, find new genes to copy and then continue evolving in their own selfish way. Therefore, viruses were using recombinant genetics long before man had thought of it.
How do viruses reproduce?
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All viruses reproduce by taking over the reproductive mechanism
of a host cell, so the first thing a virus must do is get into
a cell by passing through the cell's membrane. They do this by
means of their receptor-binding protein. These proteins
are encoded in the viruses' genetic material and they stick out
from the surface of the virion. They are attached either to the
capsid or part of the envelope, depending on the type of virus.
These proteins cause the virion to bind to specific receptors
on the host cell in a manner similar to the way a key fits into
a lock. This interaction between the host cell's receptor and
the virus' receptor-binding protein is crucial and causes the
"specificity of infection". This specificity usually
limits a viruses' infection to specific types of cells and specific
animals (or plants or bacteria) depending on the virus.
For example, HIV (the virus that causes AIDS) has receptor-binding proteins that attach to specific types of human white blood cells. Because of its specific receptor-binding protein, HIV cannot infect skin cells or lung cells so it is not infectious by touch or by breathing it in. In addition, HIV does not infect monkeys because the receptors on monkey cells are not the right shape to accept HIV's receptor-binding protein. However, a related virus, called SIV, can infect monkey cells because it has evolved a receptor-binding protein that attaches to monkey white blood cell receptors. The interaction between a viruses' receptor-binding protein and the host cell's receptor(s) is an on going battle in molecular evolution. The specificity may change as the virus evolves a new gene for its receptor-binding proteins or the host cell evolves new genes for its receptors. This evolution can produce viruses that unexpectedly switch to a new host; either a new type of tissue or a new type of animal. Once the virion attaches to its host cell it is internalized (taken inside) in a matter of minutes. Host cells internalize viruses because the host cell "thinks" the virus is something it "wants", such as food, a hormone, etc. |
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The viruses' subterfuge is aided by its receptor-binding protein, which its ancestor probably stole from the host's ancestor long ago. Once inside the host cell, the virion sheds its protective capsid and takes over the cell's reproductive machinery. Some types of viruses will actually slide their genetic material in between the genetic material of the host. Others float around inside the cell's cytoplasm (cell solution) and use the host cell's enzymes to build viruses. The exact way a virus uses the host cell varies with the type of virus. Ultimately this "genetic parasite" builds up huge numbers of "offspring" and the host cell sheds them into the blood stream, airways or other exits. Some viruses kill their host cell as they reproduce while other types quietly shed their offspring away from their host. Some viruses will even sit around quietly for years before erupting as an infection. It all depends on the specific type of virus. Regardless, the virus offspring are shed eventually and go on to infect more host cells.
OK. What's "the flu"?
"Flu" is short for "influenza". The name goes back hundreds of years when the disease was thought to be caused by supernatural "influences". Many people (including doctors who should know better) describe any nasty lung infection as flu, but only specific lab tests can give a proper diagnosis. There are several different viruses (and bacteria) which may infect the lung, but true flu is caused by orthomyxoviruses, of which there are three types, designated A, B, and C. Influenza C infects most people when they are young and rarely causes serious illness. Type B occasionally causes local outbreaks of flu and is usually confined to youngsters. Influenza A is VERY important to mankind as this is the type of virus that has caused worldwide pandemics. (Pandemics are epidemics that have spread to more than one continent.) We'll come back to type A influenza later.
| An influenza virion has about 500 "spikes" sticking out from its lipid envelope. About 80% of the spikes are a viral protein called hemagglutinin (or simply, HA). This was first identified by its ability to cause red blood cells, which carry a molecule called "heme", to agglutinate (stick together). We now know that HA is influenza's receptor-binding protein. It plays the critical role of attaching the virus to the host cell. The other 20% of the spikes are a viral protein called neuraminidase, often abbreviated NA. This protein is an enzyme that destroys a host cell molecule called neuraminic (or sialic) acid. NA might play a part in getting the virus into the cell (we aren't sure), but its most important function is that it helps the newly made influenza virions to easily escape from the host cell so they can infect others. |
Orthomyxoviruses usually infect your upper respiratory tract (throat and upper lungs) because these tissues have plenty of the receptors for the influenza virus. However, any mucous membrane will suffice as a point of entry. A common way to pick up the flu virus is to rub the moist corners of your eyes, nose or mouth after having shaken hands with someone who is shedding virus. So you don't necessarily have to inhale the cough or sneeze droplets of a carrier to become infected. Two or three days after exposure you start to shiver, have a headache and aching limbs, you feel exhausted and you get a fever (about 39oC). These symptoms are caused by your body's natural defenses (especially the release of a chemical called interferon).
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A few days later
(the older you are the longer it takes) the symptoms go away.
You're cured! This recovery is mostly due to a new group of molecules
your immune system has created to specifically fight the virus.
These specific molecules are special proteins called antibodies.
By definition, antibodies bind to specific antigens. In the case of an antibody which fights viruses, the antigen is a specific viral protein. Antibodies bind the HA, the important receptor-binding protein of the influenza virus, blocking it so it can't infect other cells. Another group of antibodies bind to the NA of the virion and may prevent the spread of further infection. Meanwhile, the cells that were originally infected are "cured" by other less well understood means. (Interferon plays a role.) The most important thing about your antibodies is that once your immune system learns how to make them, they will be there to fight off the next infection by that virus. |
Does that mean I'll only get the flu once?
Yes and no. Your antibodies will protect you from that one specific strain of influenza, but there are many other strains. If you are infected with a strain that has slightly different receptor-binding proteins, your antibodies won't recognize them. Each group of antibodies you make is specific to a single virus strain.
| If a different strain of influenza gets into your lungs, your old antibodies will not bind it correctly because the shape of a virus' receptor-binding proteins is NOT the same from one strain to another. So, that NEW strain will go about establishing a new infection with all those horrible symptoms. Your immune system will eventually create a NEW group of antibodies to fight the new strain. Once you've recovered you will be protected from that new strain, but not the NEXT NEW strain! And so it goes on throughout our lives. |
So, your immune system will protect you from becoming reinfected with the same virus (from, say a family member who caught it from you in the first place), but you will not be protected from a new strain.
How do new strains come about?
They evolve! Molecular evolution (the evolution of molecules) is a fascinating area of evolution and of prime concern to any scientist wanting to understand viruses and how they spread. All genetic material can mutate, that is change its nucleic acids. The mutations are random, but their selection is not. "Selection" is another word for how well they survive and reproduce. Selection ensures that the mutations that increase a virus' ability to survive and reproduce will be represented in even greater numbers in the next generation. Mutations are the "fuel" for evolution because they provide the genetic variation on which selection acts. This is simply Darwin's old theory of evolution by means of natural selection, but on a microscopic scale.
| All influenza viruses (all orthomyxoviruses) have RNA as their genetic material. When RNA is replicated it tends to have more errors than when DNA is replicated. These extra errors provide extra mutations upon which selection may act. That means RNA viruses (not just influenza viruses but all RNA viruses) have a high mutation rate and can evolve quickly - faster than a DNA virus or even a DNA human! Over time these mutations accumulate and eventually the virus evolves into a new strain. This progressive accumulation of individual mutations is called antigenic drift, because the shape of the antigen (the viral protein) slowly drifts into a different shape with each generation of virus. Eventually they drift so much that the original antibody can no longer bind to it. That means you can become infected with this newly evolved virus. All viruses show antigenic drift, but RNA viruses mutate faster so they drift faster. Antigenic drift is responsible for many of the localized outbreaks of different strains of influenza, especially influenza B. |
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Importantly, type A - but not B or C - undergo a kind of gene
swapping or genetic reassortment to give it its proper
name. If a cell is simultaneously infected by two different strains
of type A influenza, the offspring virions may contain
mixtures of each parents' genes! This really complicates
things and makes it very easy for influenza A to quickly evolve
new combinations of HA and NA genes. To better understand
what I mean you need to learn a little bit about how we keep track
of all this reassortment. We know of 13 different kinds of HA
and 9 different kinds of NA genes in type A influenza. All these
different kinds have evolved by antigenic drift as described earlier.
Any one virion can contain only one HA and one
NA. For example we might have an influenza A strain designated
H1N1. (We drop the "A"s at the end to make it clearer.)
Along comes another virus with different kinds of HA and NA genes,
let's say it is H3N7. If these two different virions infect the
same cell at the same time they may produce offspring not only
like themselves (H1N1 and H3N7) but also with a mixed combination
(H1N7 and H3N1).
Note that this is only a small sample of the many possible new combinations that might be made. All eight segments may take part in the reassortment. These newly created mixed genomes are very different from their parents and (probably) have never been "seen" by your immune system - or for that matter, anyone else's. This form of viral evolution is called antigenic shift, to differentiate it from antigenic drift (which occurs slowly and without a change in the gene associations). These new combinations present us with such a unique strain of virus that our immune system has to start all over to make new antibodies to combat it. |
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As if that weren't amazing enough, influenza A can infect other mammals (other than humans) and even birds! It's VERY unusual for a virus to have such a wide host range, but influenza A somehow manages this trick. It probably has to do with the fact that the virus gains entry using receptors common to many species. That means a strain of influenza A may worry one species for decades and then suddenly jump to a new species! This sudden jump, due to antigenic shift, can produce a very serious epidemic. For example, about a decade ago many seals washed up on the eastern seaboard of the USA dying from a strain of influenza A that, until then, had only been found in birds! Horse and swine influenza A have turned up in humans. Influenza A is the nightmare of science fiction - a virus that normally causes only a slight illness, undergoes genetic recombination with other species and comes back as a killer virus! Fact is, influenza A has been conducting random, unlicensed recombinant genetics "experiments" for centuries and will continue to do so regardless of our feelings on the subject.
In 1918 a strain of influenza A designated H1N1 killed over 20 million people worldwide. Forty years later, after considerable antigenic drifting and shifting, a new type A had evolved with completely different looking HA and NA. It was called H2N2 and it ran its course killing thousands of people in the USA alone. In 1968 a strain designated H3N2 appeared. It had the same old NA but a slightly new HA (H3) so it was a partial antigenic shift and was milder in its severity. In 1976 the dreaded H1N1 made a brief and frightening comeback on a military base in the USA. Although it was designated the same as the big killer of 1918, this H1N1 was slightly different due to antigenic drift.
So, what about the "chicken flu"?
Over the years virologists have collected samples of different influenza A viruses and studied them under VERY tight lab containment. In 1961 a strain designated H5N1 was discovered in some terns (birds) from South Africa. This strain was found to be devastating to chickens but harmless to humans. This avian flu didn't infect people. Or so we thought.
On the 11th of May 1997 a three year old boy in Hong Kong began suffering from severe respiratory distress. As the influenza virus reproduces in the lining of the lungs the tissues become swollen and inflamed. The lung tissue is slightly damaged but it usually heals in a few weeks and permanent damage is rare. However, it is common for young kids (and old people) to have a slow immune response and in this case the virus was faster than this poor boy's immune system.
On the 15th he was hospitalized with the two most serious complications
caused by influenza infection; pneumonia and Reye's Syndrome.
Pneumonia is an inflammation of the lungs caused by infection
with BACTERIA. Bacteria are normally kept out of the lungs by
a healthy immune system and healthy cilia. Cilia are microscopic
hairs that cover the outer parts of lung cells and
are also found among other types of cells. They sweep away any
bacteria, dust or "goo" that settles in the lung. Influenza
infections harm the cilia and thus make a person more likely
to develop pneumonia. That's exactly what happened to this boy.
Staphylococcus aureus are the bacteria most likely to take
advantage of damaged lung tissue. This bacteria is commonly found
all over the skin and mucous membranes of a healthy human but
they don't cause a problem unless they get out of control. Other
bacteria may also "dig in" during the lung infection.
I don't have any specific information about this boy, so I cannot
be specific about the severity or variety of his bacterial infection.
However, in a severe case of pneumonia secondary infections may
occur due to Hemophilus influenza and Streptococcus
pneumonia.
Reye's syndrome is a rare disorder that sometimes occurs
when a child is recovering from a viral infection, particularly
influenza. It affects mostly the brain and liver. The first symptoms
include nausea and vomiting, but this rapidly progresses to more
complex behavioral changes such as confusion or delirium. As the
liver degenerates the person's
metabolism and blood chemistry change for the worse. Most victims
of Reye's syndrome die and most of those who don't will spend
the rest of their lives dealing with the residual brain damage.
Reye's syndrome is a very mysterious disease that only affects
children and is often associated with taking aspirin (but not
acetaminophen). Naturally, many people turn to aspirin to relive
their flu symptoms but you should NEVER give aspirin to a child
under 12 that is suffering from flu-like symptoms, unless directed
to do so by a doctor after having discussed the risk of Reye's
syndrome.
On 21st of May this boy died from the complications of his flu. (Note: it is often reported that someone has "died of flu" but they usually die from the complications.) Samples from this boy were tested locally and found to be "an atypical influenza A virus". These were sent to several specialist labs around the world, who reported in August that they had isolated H5N1, avian flu, from the samples. This was the first time this strain had been found in a human! It wasn't until late November, when more cases turned up, that it made the news.
Is "avian flu" likely to become a pandemic?
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Probably not. (Notice I said "probably"). A pandemic
would result only if the avian flu could pass from one
human to another. Although the results (so far and to my knowledge)
cannot rule out that possibility, there is certainly no evidence
that H5N1 can pass from human to human and I would expect
to have seen some evidence of that by now. My opinion is based
upon the results of a few lab tests reported by the Center for
Disease Control (the experts) on December 27th. Further data may
change my mind, but so far I'm not worried and here's why.
All strains of influenza produce strain-specific antibodies in the people who become infected with it. (Remember?) People infected with strain H5N1 will have antibodies in their blood that bind the H5N1 antigens. We say they are seropositive if they have the specific antibodies. The first person to die of the avian flu (complications!) had contact with chickens so we see clear evidence for a bird-to-human link. (The first of its kind!) Not surprisingly that boy had antibodies to H5N1 - not enough to save his life but enough to show that he was seropositive. Now imagine you were part of a family with a 3 year old boy suffering from flu. Considering the mess and awful hygiene that goes with children of this age, along with the supervision, attention and contact needed to make the child comfortable, it's easy to understand why people in the family should be at high risk of catching the flu. The good news is that none of the four members of his family were seropositive, all four were seronegative for H5N1. Therefore, they didn't catch avian flu from the boy even though they would have been prime candidates. |
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However, one of the 54 health care workers who came in contact with the boy was seropositive for H5N1 and that person does not recall any exposure to poultry. This might be taken as evidence for human-to-human transmission of the virus! Or it might be taken as evidence that the health care worker can't remember when she handled a chicken. The interesting thing about antibodies and these tests is that you usually remain seropositive for many years, often all your life. How many people do you know who can swear that they've never touched a chicken? Besides, when they tested 63 people in the same neighborhood but otherwise not involved with the boy, they found one that was seropositive. Although these numbers suffer from a lack of statistical rigor they hint that one might be seropositive from handling an infected chicken but not recalling it. Also, it's possible to be seropositive without being infected. Why would someone be seropositive without being infected? I don't know, but I do know that tests like these can give false positive results. The tests can say you've been exposed to the strain when in fact you have not. All serology tests (as these are called) have some level of false positive rates and new tests (like this one) often have very high false positive rates.
Contrast this figure (one positive in 54) with the fact that they found 5 seropositive poultry workers among 29 tested (that's 17.2% positive). They also tested 18 pig farmers and found none of them were seropositive. Looks like you are more likely to get avian flu from chickens than from people or pigs. That's why I'm not too worried.
Another reason for optimism concerns the viral genes isolated from the few cases of avian flu in humans. Analysis of their gene sequences show that they are all avian with no sign of genetic reassortment with a human influenza. That's reassuring because if they had found even one gene segment from a human influenza it would mean that someone had been infected by both the avian AND a human flu and that the mixed offspring viruses could be evolving towards a human-to-human means of transmission. (It's difficult to go into the details of how you can tell an avian flu gene from a human flu gene, but suffice it to say that the specific gene sequences are compared and used to identify the species of origin.)
I suspect that if avian flu is jumping from one human to another it is doing so very poorly because all four members of the family are seronegative and the very low number of seropositive people in contact with the child is similar to the frequency of seropositivity in the local population anyway.
As of the 21st of January 1998, there have been 18 confirmed (by serology tests) cases of H5N1 in humans. Six of them have died, so this is a pretty deadly virus, similar to the virulence of H1N1 from 1918. Ten people have recovered from their infections and been released from hospital. The remaining two are still in hospital, one critically ill and the other in satisfactory condition. In all cases contact with chickens has been the likely route of the infection, not human-to human. There have been no new cases of H5N1 in over a week. So it would seem that while H5N1 has all the "killing power" of the monster H1N1 it isn't spreading from human to human so it isn't likely to become a pandemic. We are now reaching the end of the flu season and I think it will end without a big outbreak of avian flu. I'm not worried. However, there is no telling what these viruses may come up with next. After all they are masters of evolution (because they cheat!).
If you have a comment or question about influenza feel free to
send a Letter to the Editor.
I can't promise to answer all your questions or address all your
comments, but I'll post a few particularly good ones here.
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Dr Jamie Love, the editor of this website and all of Science Explained, has written several self-study science courses specifically designed for home schoolers and other distance learners. These courses are "hypertextbooks" - delivered over the internet and read on your computer, just like web pages.
To organize and distribute these hypertextbooks, Jamie created Merlin's Academy - a (non-accredited) "virtual school". Merlin's Academy sells self-paced, self-learning hypertextbooks that teach Alchemy (actually, Chemistry ),
Astronomy and
Genetics in a fun and unique way.
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