Suppose you could look into this baby's future, predict the diseases he was most likely to
catch during his life, and then protect him from them by vaccination.
This program is about a unique experiment in medical science, which could make that
dream a reality.
Physicists and scientists all over the world are collaborating.
It could revolutionize medicine.
In the fight against disease, we depend on unseen heroes, patrolling white cells sniff
around in blood and tissue, mopping up foreign dirt and our own debris like this dead cell.
During three million years of evolution, we've built up a complex system of defense against
microorganisms.
White cells keep watch for invading microbes.
These black dots are bacteria.
It's a direct attack.
There's another line of defense, less direct, but just as deadly.
That patrolling cell sees an invader, it passes the alarm to a whole army of other cells.
At the alarm, some of these cells turn into chemical factories and move into the attack.
They produce molecules of antibody, which poison the invader.
But how is a foreign cell recognized?
Each of us carries a system of markers on the surface of our cells, over 6,000 of them
protein molecules called antigens.
When one cell meets another, it sniffs at these identification markers.
If they're different from our own, the alarm is raised.
Antibody molecules fasten onto these markers like a lock and key.
These antigens are chemical fingerprints on our cells.
Even at that microscopic level, we're different from each other.
These antigens, these markers on our cells, could be the key to our survival and new knowledge
of them may lead to a breakthrough in preventing disease.
Jean Dosset is one of a team of scientists around the world who are trying to tap the
secrets on the surface of our cells.
In his deep freeze, he keeps over 3,000 samples of human tissue, living material for an experiment
to discover what makes our cells unique.
But 25 years ago, he was working on blood diseases.
In a sample of blood from one patient, he saw white cells clumping together in a sticky
mass.
It meant the patient was attacking them.
He'd produced antibody against these cells, just as if they were germs.
Was this the cause of the disease?
Was the patient destroying his own white cells?
Dosset decided to publish.
His paper set off a train of events around the world with unexpected consequences.
A team at Stamford found similar antibodies, but only in the blood of certain patients.
Rose Payne noticed they had one thing in common.
All these patients had been given several blood transfusions.
Their bodies were attacking white cells from the donor that were recognizing a foreign
type of cell.
Let's talk about it tomorrow at the meeting, shall we?
This had been looked for back in 1924 without success.
And suddenly, it fell into the lap of a number of scientists by an indirect route, really.
They were not looking for white blood cell types.
They were looking for self-destruction in an individual of his own white blood cells
by an antibody.
Rose Payne found the where white cell types.
They were like the ABO blood groups on red cells.
It explained why some patients reacted badly to blood transfusions.
They were making antibody against the donor's white cells.
Rose knew this was uncommon.
So did it only happen after many transfusions?
Her question was soon answered by an event in Holland.
A woman reacted to a blood transfusion in a Leiden maternity hospital.
Jan van Groot investigated.
Although she had very strong antibodies, we had no records from her while she was living
in Leiden that she had received any blood transfusions.
So we went over to her and said, well, you have just a very nasty experience.
And it is caused by antibodies in your blood, and we know that these antibodies occur only
after many blood transfusions, but we can find no records of you having any blood transfusions.
How is this possible?
And she looked at this in horror and said, well, listen, I just got one blood transfusion.
The first one in my life got very sick, and I don't want to hear any talk about blood
transfusions.
And then a little light started to burn, and we realized that perhaps all these experts
before us who said that these antibodies could occur only after blood transfusions and had
actually said that they could not occur after pregnancy, that these experts were wrong.
Van Groot discovered that about one third of pregnant mothers already have antibodies
in their blood, which could attack white cells in a blood transfusion.
These antibodies have been formed against their babies.
A child developing in the womb represents a massive invasion of the mother's body by
foreign cells.
As the baby grows, its cells divide and die.
Dead cells from the fetus go through the placenta and into the mother's bloodstream.
The mother will recognize on these bits and pieces, for instance, also the genetic information
which comes from the father of the child.
And even if she knows the man very well, she will recognize this.
Her body will recognize that that's foreign and say, hey, stop a moment, and she will
make antibodies against these bits and pieces.
Now, in this case, these antibodies will not, generally speaking, reach the unborn child,
will not do it any harm.
It will stay in the mother for many, many years, 10, 20 years, even after the last pregnancy.
Pregnant mothers make antibody which is ideal for white cell typing.
Each antibody fits a specific type of marker on the baby's cells inherited from its father.
The baby isn't harmed, but its mother provides a treasure trove of tools for detecting these
new cell types.
Research took off.
Mix a patient's cells with a set of antibodies, and you get a set of reactions.
But how could these reactions be organized into groups, like the blood groups?
How could they be used to classify types?
There was still another problem to solve.
It was a problem in statistics.
It called for computer techniques.
In 1961, Walter Bodmer, now Professor of Genetics at Oxford, was working at Stanford with his
wife Julia.
They joined the growing band of white cell typers.
In fact, almost the first thing that we did when we started applying some of these statistics
to this, Julia got a little program and popped the first two antigens that we discovered,
which we now call A1 and A2, and these are types, they're like blood types, like the
ABO blood types, but there are just a lot more of them, and they're a lot more complicated.
So white cell typing began in earnest.
Soon they had typed the world.
There was enormous variety.
They called the system HLA, human nucleoside antigens, molecules which we cannot see, invisible
even to the electron microscope, detectable only by complex biochemical processes.
They make our cells unique.
Blood groups, groups on white cells, groups on tissues, groups which are important for
transplantation, are all inherited.
You get the information for them from your father and from your mother.
And when you have ways and means to recognize these groups, you can classify people.
In blood transfusion, everybody knows that.
I am blood group O. No, but you are blood group A. We have been classified in O and
A. Now with these white blood cell groups, things are a bit more complex because we do
not have four blood groups as we have in blood transfusion, but we have millions of them.
There are millions of different combinations, some very rare, some more frequent, but even
the most frequent does not occur in more than, say, in one out of a hundred Englishmen or
Dutchmen, whatever you look at them.
But how do we acquire these antigens, these fingerprints on our cells?
We are all unique, even at the level of our cells we are different.
We're built out of information inherited from our parents.
The color of our hair, our eyes, our skin, the information for them is carried on our
chromosomes.
We're programmed by our genes.
Even those markers on the surface of our cells are inherited.
The genes for them have been located deep within the cell on one tiny area of a single
chromosome, on chromosome 6.
At first they found two groups of antigens.
We're classified by A and B types, two of each inherited from our parents.
But the number of types is enormous.
More than 20 of each have been found.
There are over 30 million possible combinations.
There's not much chance of two people being exactly alike.
If our cell types are so different, could that be why we reject transplants?
In Paris, where it all began, Jean Dosset ran an experiment with human volunteers.
He knew white cell typing was important in blood transfusions, they're a kind of transplant.
So is a fetus, an invasion of the mother by human cells.
Since the mid-60s, Dosset and other workers have experimented with skin grafts, also a
form of transplant.
In the family, white cell types may be the same.
Dosset has been swapping skin grafts between parents and children to see if matching white
cell types would delay rejection.
He found that a skin graft would survive much longer if white cell types were closely matched.
And it was even more successful if blood groups matched as well.
It was the same for kidney transplants.
Especially between brothers and sisters, there could be a hundred percent success.
So HLA matching became an important weapon in the transplant surgeon's armory.
White cell types were tissue types, they classified human tissue.
The scale of these operations suddenly grew.
This is uro-transplant in Leiden.
Just a minute, I have to write it down, five years old, female, and what is the blood group?
AB, well that's very rare, and the typing, A1, B17, BW35.
But HLA types vary enormously.
When a kidney becomes available, it's difficult to find a matching patient and time is short.
Information about their tissue types is now computerized.
Data on patients is immediately accessible.
There's a worldwide network of linked operations.
I checked our list here in uro-transplant, but unfortunately we have no suitable recipients
for these two kidneys.
And I already contacted our sister organizations, but they don't have recipients either.
So I made a telex to Teheran, this organization is working with us too, and they have two
suitable recipients and they accepted for these two kidneys.
I advised them to make contact themselves for the medical data and organizing the flight
and so on.
A patient in Teheran saved by an American kidney.
HLA research was already paying dividends in medicine.
It had begun with blood transfusions.
Now it was saving patients with kidney disease.
But why should HLA be there?
Around the world, research was continuing.
Scientists were working together, they'd formed an HLA clan.
They were trying to pinpoint the role of these markers on our cells.
Clues came from work on lowlier creatures.
In mice, there's an equivalent system of types.
They control the survival of grafts between animals.
In 1964, a clue emerged from a New York laboratory.
Frank Lilly noticed that mice with a certain tissue type were vulnerable to a form of leukemia
caused by a virus.
If they had that type, they died when exposed to the virus.
If not, they survived.
Was HLA linked with human disease?
No one could find out.
A connection turned up unexpectedly in 1971.
Not with leukemia, but with a painful form of rheumatism.
Brian Hill has ankylosing spondylitis.
The bones of his spine have fused together.
It's a disease which is generally unknown, except to its sufferers.
No one knows what causes it, and there's no cure.
Brian has had to give up his job.
He can no longer look to left or right.
All they can do is keep the patients mobile with physiotherapy and treat them with anti-inflammatory
drugs.
Like most forms of rheumatism, ankylosing spondylitis has been studied for over a century,
but no headway has been made.
Even diagnosis is difficult.
The symptoms can be hard to recognize, especially in women.
This patient was in and out of hospitals for years before doctors diagnosed her disease.
When I was a child, I remember I was going into the local hospital to see various specialists
and they all said there was nothing to be seen, nothing to be found, and then of course
when I was in the army, the same thing happened, I was in and out of physiotherapy departments.
Then when I was working, I was a typist and I found that it was great pain, very painful
indeed to work my typewriter and to bend down to the filing cabinet.
It was agony.
And of course again, I think I was regarded as being a bit of a lead swinger, which is
rather unfortunate, and then eventually I had to give up work.
In 1971, a team at London's Westminster Hospital made an unexpected discovery that was to shake
the world of rheumatology.
How are you feeling?
Well, a little better today compared with yesterday.
Derek Brewerton decided to check the tissue types of his patients.
Straight off, we found that a particular component of a tissue type, an HLA antigen B27, which
is present in 7% of the British population, was found in 96% of patients with ankylosing
spontalitis.
Now obviously, such a result is much too good to be true, and we worried from the beginning
that it might be a false result.
Could it be an accidental finding?
Had drug treatment affected the tissue types of his patients in some way?
He decided to test near relatives.
Most of them had no symptoms and had never been given drugs.
Did they also have the B27 type?
If the marker was being inherited in the normal way, half of them ought to be having the same
B27.
And much to our relief, 32 out of the first 60 relatives we looked at had the same marker.
It was being inherited in this normal way.
So therefore, we had a genetic marker of remarkable power.
If you were born with B27, you were over 300 times as likely to develop spontalitis as
if you were born without it.
At about the same time, working independently in Los Angeles, Paul Terasaki was finding
similar results for ankylosing spontalitis.
He studied different racial groups.
In Japan, the B27 antigen is almost non-existent.
Very few people have it.
And yet, essentially, all the patients that have ankylosing spontalitis that are Japanese
have the B27 antigen.
The connection was always the same, whatever race he checked.
We looked at some Negroes and found that even though the disease is rare, patients that
have ankylosing spontalitis tend to have B27.
Tissue typing was soon proving useful to doctors.
Would you like all to come in?
It could confirm diagnosis in doubtful cases, especially in women.
But its real value lay in research.
Doctors began studying family patterns of disease.
Now, Mrs. Kennedy, thank you very much for coming with your daughters.
Now, you've had spontalitis, a painful back condition, since you were 20.
I understand that you have a sister who has spontalitis and symptoms very like yours.
Have you been able to compare notes?
Well, very similar to me.
I can't get out of bed in the morning.
If you get over tired, you just can't move, you know, and crawl up the stairs sometimes,
can't walk, you know, can't get up them.
Mrs. Kennedy's daughters are also B27 positive, but they have a puzzling assortment of symptoms.
I don't have the spontalitis, but I have psoriasis, a skin complaint.
Have you had any rheumatic symptoms at all?
No, none at all.
Could you show me your arm and see what this...
Just one patch.
I see.
Now, what is this like?
It's not infectious, but what's it like as far as you're concerned?
It doesn't irritate or it doesn't really bother me, apart from getting embarrassed
about it and people seeing it.
You've had no aches or pains or real discomfort with this at all?
No, no.
Now, Lynn, you've also had arthritis and inflammation of the eyes.
Could you tell me what an acute attack is like?
Well, it looks red, but the pain's quite bad and, you know, I have to sort of deal with
it quite quickly.
How long may an average attack last?
About three months, three or four months.
But you've also had arthritis in the joints of your limbs.
When did this begin?
When I was working.
When was that?
When I was 17, 18.
And what was your work and how did you get on with it?
Well, I couldn't keep it up.
I was hairdressing.
Symptoms like these were often seen in the same family, but why?
Was Lynn's arthritis a complication of the disease?
What was the connection with psoriasis?
Eric Brewerton wondered if the connection was the B27 marker.
Well, we knew that a third of patients with ankylosing spondylitis may develop arthritis
and acute inflammation of the eyes, and yet most patients who have arthritis don't have
ankylosing spondylitis at all, and it doesn't really behave like a complication.
So we wondered whether the connection between the two disorders might be inherited, in which
case if we looked at people who had arthritis without any rheumatic disease at all, then
we might find a marker there.
And Moorfield's eye hospital kindly sent us 100 patients as they turned up at their casualty
eye clinic, and true enough, over 40% of the patients with acute arthritis without rheumatic
disease had the same marker B27, and this meant that a Londoner born with B27 was 20
times as likely to end up at Moorfield's with arthritis as the rest of the population.
It seems we can inherit a susceptibility to disease, but many people with B27 remain healthy
all their lives.
There has to be some other factor.
Everything in the environment must trigger off the disease.
Evidence for this trigger came from an unexpected source, a report by a ship's doctor of an
extraordinary event on the USS Little Rock.
On the 2nd of June, 1962, the ship docked at Trieste, 1,200 marines went ashore, among
them were the two chefs.
As often happens on such visits, one of them caught tummy trouble.
He went down with Shigella dysentery, but anxious not to miss the fun, he didn't tell
anyone.
Later, he helped prepare a barbecue and spread dysentery among 600 of the crew.
But four weeks later, 10 of them developed a painful form of arthritis, so severe they
had to be invalided out.
The ship was a perfect floating laboratory, 10 neat case studies for tissue-typing sleuths.
Ten years later, in California, Andre Carlin read the report and decided to follow it up,
but first he had to find the patients.
The major problem was that the naval authorities felt, perhaps naturally, that a lot of this
information was confidential, and they were a little reluctant to give us too much information,
but eventually, with help from various departments in the United States Navy, we did manage to
contact at least one of these individuals, or at least his next of kin, and then going
through this individual's mother, we managed to find the first patient, and then during
the next months, found five of the ten.
And when we came to HLA type these, to our great pleasure and excitement, we found that
four of the five were B27 positive.
So holiday tummy might sometimes cause arthritis.
After certain infections like Shigella dysentery, you've a one in five chance of developing
arthritis if you're B27 positive.
We all respond differently to our environment.
Tummy trouble from incautious eating may be more disastrous for some.
It can lead to reactive arthritis.
At the Westminster Hospital, Derek Brewerton is assembling a team to investigate how a
virus could interact with B27 to cause disease.
Could ankylosing spondylitis also be triggered by infection?
This is the main problem with ankylosing spondylitis.
We haven't yet found an infection to account for this disease, and therefore, I think the
next stage is to look in the gut and elsewhere, possibly, for a source of these infections.
Jack, how do you think we should proceed on that evidence?
Well, in the patients who get an acute arthritis following these gut infections, there is evidence
that they have immune reactions going on in their bloodstream.
It's as if the gut is the trigger, and that gets something going in the bloodstream which
might then cause the damage in the joints.
Tissue typing won't help patients, and we may be a long way from finding a cure.
But if scientists could isolate a virus, then one day it might be possible to vaccinate
against these crippling diseases.
Preventing diseases like rheumatism seems an impossible goal, but doctors are beginning
to learn that the diseases we get are not pure charts.
For it is not only rheumatism that is implicated.
Anne Beals has two children with diabetes.
Every morning she has to prepare insulin shots for them.
Without it, their blood sugar levels would become dangerously high.
Philip was ten when his diabetes was diagnosed, Andrew only five.
When the illness begins in childhood, it's always more serious.
They will have to take daily shots of insulin for the rest of their lives.
No one knows what causes diabetes, or how it's inherited.
It does seem to run in families.
The Beals have a daughter.
She remains well, though both her brothers are affected.
But often there is no family history.
Doctors believe that diabetes could be triggered by a virus.
Some children develop it after catching mumps.
Another clue is the age when the illness begins, most commonly at five and eleven, soon after
they start a new school, when children are exposed to a whole new set of infections.
Though the evidence points to a virus, there's no proof.
Now some of those mysteries are beginning to be resolved.
In 1974, a Liverpool doctor heard about B27 and ankylosing spondylitis.
He saw implications for diabetes, strange family patterns, possible virus trigger.
Andrew Cutworth began a survey of families in the Liverpool area with two or more affected
children.
The Beals were among them.
He tissue-typed whole families.
He also took a complete family history of disease.
Do you think that, in the case of either Philip or Andrew, that they had been ill with anything
immediately prior to them developing the diabetic symptoms, or did they have mumps, for example,
or anything like that?
No.
None that I can actually say that that was it.
But Philip, the only illness he didn't have, he had all the childhood ailments, was mumps.
And he was in contact.
Yes.
And Andrew's not had mumps.
What relationship did the contact with mumps have to the time that he started to become
thirsty, for example?
It's hard to say, because you tend to think that must have been it, but I think perhaps
a month or perhaps two before, we really noticed that he was...
Yes, but as far as you know, he didn't actually have mumps itself.
No, no, he didn't have mumps.
Yes, I see.
The other thing I would like to ask you, if you don't mind, is whether you know of any
family history of diabetes?
Well, my husband's cousin was 15, and that's the only one we can trace.
Yes.
And is he on insulin?
Yes, yes.
I see.
Is there anybody in your family who has anything wrong with their thyroid gland, did you know?
No, no.
Or pernicious anemia?
No, probably your father, my husband's father.
Oh, really?
He's got pernicious anemia.
That's very interesting.
Yes, we didn't think of that.
Sometimes we see pernicious anemia and diabetes, or this type of diabetes occurring in the
same family.
So that's very interesting.
I didn't hear that.
Could tissue-typing families like the Beals help to sort out this mass of information?
One thing was soon clear.
Diabetes is not a single disease.
It takes two forms.
I think what the HLA studies have shown quite conclusively is that here we now have scientific
evidence for these two major types of diabetes being quite separate, separate in their etiology
and with the HLA association being only found with the juvenile onset type and not with
the more common mild late onset diabetes.
Philip and Andrew had helped to provide one clue, but the picture emerging from these
family studies was much more complex than the one found by the rheumatologists.
There was no single tissue type acting as a marker for the disease.
There were three, B8, B15, and B18, and there were not such accurate markers as B27.
Nevertheless, a child with any one of those types was two or three times more likely to
develop the disease.
They were getting close to a gene for diabetes.
By HLA typing the parents as well as the children, both the affected and the unaffected children,
we were able to establish without any question of doubt whatsoever the actual identity of
this small piece of HLA chromosome in the affected children.
For example, in this family here, the mother also had insulin-dependent diabetes, and there
were three boys, and the interesting thing is that in this family the three boys have
inherited the same pair of A and B antigens in each case.
The 37 here, for example, has been inherited from the father, and the 2818 haplotype as
we call it, that's an A and a B antigen, have been inherited from the mother.
So significant was this that it provided the really conclusive evidence that there must
be a gene in the HLA chromosomal region conferring the major susceptibility to this type of disease.
But what hope does this hold for the future?
How can it help research?
The next step will be to hunt for triggering viruses to study children who develop diabetes
and look for evidence of some recent infection.
Doctors can already begin to identify the susceptible child.
One day we might perhaps prevent diabetes by vaccinating babies at risk.
In the last four years, the HLA net has been thrown wider.
Paul Terasaki set up a tissue typing production line in his laboratory in Los Angeles.
It can handle hundreds of samples a day.
Every single disease which is ever seen at Terasaki's hospital is checked for association
with HLA.
More and more are implicated, rheumatoid arthritis, skin diseases, anemia, liver disease, diseases
of the thyroid gland, poliomyelitis.
Most of them have been a complete mystery to medical science with no known cause or
cure.
As the list grows, one thing becomes clear.
We are not born with equal chances of catching diseases.
The genetic dice are loaded from birth or even before.
The diseases we catch are the result of a complex interplay between genes and environment.
Some of this knowledge could be applied now.
In third world countries, the benefits could be immediate.
For recently it's been found that HLA is associated with leprosy.
It's a disease which is still endemic in much of the world.
It can be prevented, but the drug is expensive and the side effects painful.
No one would give these drugs to the entire population of India or the Sudan.
Most would not need them.
But leprosy does run in families.
By tissue typing, doctors could identify the child at risk and protect him from the disease
by drugs.
Applications to western disease are not yet so promising.
But recent research has brought new knowledge of the HLA system through skin graft experiments
on volunteers.
We had been looking for ways and means to keep this skin graft going for a longer time
because we knew every day we won and we could prolong the skin graft survival.
If we would apply that to kidney grafting, it would mean that the kidney graft would
survive not one day, but a year longer.
Every day counts in this game.
We were doing these studies and then one of the ladies came in.
And we thought that we had fixed things in a certain way that the skin graft should slough
off after say between 12 and 14 days.
But at 14 days she was fine and at 15 and 16 and so on.
And only when it was 22 days, the skin grafts left off.
And we could not understand that with the information we had at that time.
Her blood cells were revealing new secrets about how the system worked.
She'd been given a skin graft which didn't match her A and B types, yet the graft survived.
She'd been accidentally matched for a new type as yet unknown to scientists.
It turned out to be more important for transplants and a much more powerful marker for diseases
like diabetes.
The gene for this type might control immune response.
In disease it could make that response too high or too low.
Scientists are finding more and more types of antigens on the surface of our white cells.
They're locating more and more genes on chromosome 6, getting closer to the key to how we fight
disease.
The A and B genes are linked to two more, C and D. The newest, IA, could be the ones
to switch the immune response on or off.
These genes could be involved in one of the most baffling diseases of the 20th century,
in multiple sclerosis.
It's a disease where patients mistake their own tissue for something foreign.
Their white cells attack the protective sheath around the nerves in the brain and the spinal
column.
No one has any idea why.
For years Mary Quinn has acted as guinea pig in a whole series of research projects to
try and find the cause of her disease.
But despite all the money and effort which has been poured into research, and although
many scientists have been attracted into the field, multiple sclerosis has refused to yield
its secrets.
What percent certainty is it that it's virus-induced?
Oh, none at all, I mean it's...
In fact all, virtually all the things that, when people have claimed to find a virus,
in the end it hasn't been reproduced.
This team of scientists based at a hospital in Sussex joined the hunt for a link with
HLA.
They found that 30% of patients had the A3 type, 40% had B7, it wasn't very significant.
The new D types provided a much more powerful marker, 60% of patients had D2, they were
getting closer.
But now they found a new type, which only appears on certain white cells, on cells which
produce antibody.
They called it BT101.
They found it in over 90% of patients.
At last, after decades of fruitless research into multiple sclerosis, scientists have gained
a foothold.
They can begin to compare patients who have the disease with people who have the same
high-risk marker yet remain well.
They can try to pinpoint the trigger which might have set off the disease in people like
Mary.
And it might well be that we find that all people who had this particular susceptibility
had some particular infection early on in life, whereas people who had that same infection
who don't have the genetic susceptibility would never have been at risk.
And so one of the things that we hope to do in the future is to compare all people who
have this particular genetic susceptibility marker and divide them into two groups, those
who've got MS and those who haven't got MS, and see what important differences we can
spot early on in their lives, which might give us a clue as to what has been this important
infection, if that's what it is.
There's one thing about, when you say about the diseases and things, there is one thing
I have.
The only thing I've had, the only thing, is when I was a child I had nothing at all, childhood
things.
But I did have, when I was about 18, 19, I had hepatitis.
Well that is the only thing I've ever had, as far as that is the only thing I've had.
Well this is just a sort of clue that might turn out to be important.
I mean, whether it'll be hepatitis or not one doesn't know.
There'll be no magic cure for Mary, but the connection with HLA is opening up new fields
of research.
A team in Copenhagen decided to investigate what could be wrong with the immune response
of patients.
They added blood samples to viruses like measles in a special culture dish.
In normal people, white cells were mobilized into action, producing a halo around the virus.
In the multiple sclerosis patients, there was no movement and no halo, their white cells
did not respond.
Platts and his colleagues then treated patients with a drug which was known to step up the
immune response.
They tried again.
This time there was a reaction.
The patient's immune response to the virus had been altered, their white cells attacked.
It couldn't produce a cure, but the Copenhagen team are beginning lengthy trials to see if
the drug could slow down the course of the disease.
All this is very much for the future.
For the present, they're trying to find out how HLA could be involved in the disease.
There are plenty of theories, none proved.
One idea is that a virus might gain a foothold by mimicry.
Usually it's given away by the molecules on its surface.
But what if those markers look like our own?
Then patrolling cells may be fooled.
The virus could lodge in our cells for many years, then trigger off a response, perhaps
even to our own tissue.
The scale of research has become enormous.
With so many teams involved in the HLA work, Arne Sveigor decided to set up a register
in Copenhagen to coordinate research.
Everyone agreed to participate.
Since 1964, HLA researchers have combined their efforts, freely exchanging data.
Every disease is being studied in every continent of the world.
Now, even psychiatric illness is included.
Schizophrenia and manic depression have been added to the list.
Every single result is fed to Sveigor, both positive and negative, and stored in his data
bank.
In five years, they've built up a world picture of disease.
We've only recently become aware of HLA in man and the extraordinary role it plays in
our survival.
But scientists believe it could be one of the oldest gene systems, dating right back
to the beginnings of evolution, when the first multi-celled organisms evolved.
Organisms like it are found in almost all animals, even reptiles.
There could be a more fundamental role for these molecules in our cells.
When a complicated organism develops, the cells have to get together in appropriate
ways.
An organ has to be formed, the liver or other sorts of organs.
And the cells have to know when they're recognizing each other.
And one way that this can happen is by having the right sorts of molecules on their surface.
And we think that perhaps some of the products of the HLA region serve this function of telling
cells when they're recognizing each other in the proper way.
And so it's possible that really quite early on in evolution, when one had a transition
from simple single-celled organisms to more complicated organisms, which have many different
cells that have to get together, that HLA, or systems at least very like it, evolved
to serve this role of recognition, and that it was actually that role then that was later
used during evolution to develop the immune responses we see it now, and to produce some
of these many effects of the HLA system that lead to its association with diseases, the
things that we see now.
I personally think that the disease associations, as we call them, that certain people with
certain disease get a certain HLA type more frequent than others, is more or less an accident,
is a fringe effect.
And that the thing which the HLA system is really for is that it is a kind of a central
brain which recognizes foreign from self, which is extremely important in combating
infections, viral or otherwise.
And we have recently, we have been able to really provide very solid proof for that,
for instance for leprosy, and all probability for smallpox and a number of other diseases.
HLA may be the key to our continuing survival.
The gene system which enables us as a species to survive infection.
Yet these genes also make us vulnerable to degenerative diseases like rheumatism and
arthritis.
But perhaps disease may not be so inevitable now that science has made the link between
that vulnerability and our genes.
I think whatever advances we make with the help of B27 there will still be forms of arthritis
that do not fit in closely in this disease area and they may continue to be a problem.
But it would seem that now that we know why certain people get the disease because of
B27, we'll be able to learn more of the mechanism and understand why a certain precipitating
infection would be associated with disease and perhaps in the future we would either
be able to vaccinate against the possible infective agent or probably more realistically
use blocking antibodies or some other immunological manipulation to prevent people with that gene
developing an arthritis just because they come across an infection.
It's too soon to know how to protect these children from diseases like rheumatism and
multiple sclerosis but already we can identify those at risk and dream of prevention.
We know that susceptibility is inherited, that the way each of these children will respond
to a hostile environment is programmed in their genes.
Now scientists are locating those genes and learning how we fight disease.
Research began with white cell types.
These types were a key to our individuality and they showed our vulnerability to disease.
Now scientists believe there's a broader role for HLA.
It could be a blueprint for survival.
Personally, I think that the main importance of HLA lies in a role that it plays in defending
us against viral and bacterial infections.
This still is a concept which we have to prove.
We have evidence but you have to prove it definitely.
If this is really true, then I think one might say that we are here because HLA was there.
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