Humans With Green Skin Could Live Off Sunlight.

Let's hear it for the bad guys!

Hey guys – let me introduce myself. My name is ERVWE1. Oh by the way, I’m a virus. Now some of you people might think that comes with some negative vibes, like evil! Or it means I can’t be alive. But I feel pretty much alive, in a wrinkly kind of way. Don’t get me wrong. I had those same ballsy feelings you guys probably have, maybe kind of a long time ago, could have been twenty or maybe even forty million years ago, in the time of my misspent youth. Boy – or maybe I should say girl – who’s to say? Daughter viruses some of you call them, so maybe it was more kind of an eggsy than a ballsy feeling, but let me tell you, folks, those were the days. Hey, man – I went under a different handle back then. I was HERV Dubya the Barbarian. I was the slayer!

I don’t suppose you guys ever fought a pandemic kinda conflict. So I wouldn’t expect you to share those old bad-guy buddy feelings. But all I was doing is following the good old imperial directive. You gotto go on out there and make a lot more little viruses like yourself! But, you also got to realize I was just a kid letting off steam. I’ve grown up a lot since then. Honest – I’m one of the good guys now… At least I think I am… For the moment kind of… Just so long as one a them good old buddies don’t cosey up to me and swap a little rejuvenating information…

Hmmm!
 
Why We Don’t Lay Eggs

Explanation the ERVWE1 locus...

Among the many animals that live on land, and in the oceans, only the mammals don’t lay eggs. They protect the developing foetus within the mother’s womb for lengthy periods, so that it is born into the world as a fully formed baby. To achieve this, mammals have evolved a special organ capable of nourishing the foetus in the womb, and all the while protecting it from being attacked by the mother’s powerful immune system. The organ that makes this possible is the placenta. We humans have the most specialised placenta of all the mammals, more deeply penetrating into the mother’s womb, and with an exquisitely fine membrane, only a single cell thick – much finer than tissue paper – that separates the mother’s blood from that of the foetus, and through which this all-important nourishment takes place. But here the wonder increases. This ultra fine membrane is very unusual – its cells are fused together so their membrane have dissolved away, making up a single monolayer. Animal genes cannot fuse cells in this way. How then does our human placenta, vital to the miracle of every human birth, manage to do this?

It does so with the help of very special types of viruses, which have been incorporated into our chromosomes. The discovery of these viruses has shocked the world of science, since scientists are more familiar with viruses as the cause of infectious diseases, such as AIDS and flu. But now we know that these viruses really are playing a key beneficial role in our human life story. They are known as human endogenous retroviruses – in the scientific jargon, HERVs – and they have, in essence, become an integral part of us through an evolutionary mechanism known as genetic symbiosis. More remarkably still, these viruses have a genetic make-up that is very similar to the virus HIV-1, notorious as the cause of AIDS.

The wonder of the viruses and the human placenta doesn’t stop there. Our human chromosomes are full of similar viruses, and genetic sequences that come from them. They are an integral part of our genetic makeup. Two of the three placental viruses make proteins, known as syncytins, that enable the placental cells to fuse, and they also help the placenta to stop the mother’s immune system from damaging the foetus in the womb. A Swedish pathologist, Erik Larsson, has recently discovered that these syncytins are also playing some important, but as yet unknown, function in the normal human brain.
 
Frank Ryan said:
Explanation the ERVWE1 locus...

Among the many animals that live on land, and in the oceans, only the mammals don’t lay eggs. They protect the developing foetus within the mother’s womb for lengthy periods, so that it is born into the world as a fully formed baby. To achieve this, mammals have evolved a special organ capable of nourishing the foetus in the womb, and all the while protecting it from being attacked by the mother’s powerful immune system. The organ that makes this possible is the placenta. We humans have the most specialised placenta of all the mammals, more deeply penetrating into the mother’s womb, and with an exquisitely fine membrane, only a single cell thick – much finer than tissue paper – that separates the mother’s blood from that of the foetus, and through which this all-important nourishment takes place. But here the wonder increases. This ultra fine membrane is very unusual – its cells are fused together so their membrane have dissolved away, making up a single monolayer. Animal genes cannot fuse cells in this way. How then does our human placenta, vital to the miracle of every human birth, manage to do this?

It does so with the help of very special types of viruses, which have been incorporated into our chromosomes. The discovery of these viruses has shocked the world of science, since scientists are more familiar with viruses as the cause of infectious diseases, such as AIDS and flu. But now we know that these viruses really are playing a key beneficial role in our human life story. They are known as human endogenous retroviruses – in the scientific jargon, HERVs – and they have, in essence, become an integral part of us through an evolutionary mechanism known as genetic symbiosis. More remarkably still, these viruses have a genetic make-up that is very similar to the virus HIV-1, notorious as the cause of AIDS.

The wonder of the viruses and the human placenta doesn’t stop there. Our human chromosomes are full of similar viruses, and genetic sequences that come from them. They are an integral part of our genetic makeup. Two of the three placental viruses make proteins, known as syncytins, that enable the placental cells to fuse, and they also help the placenta to stop the mother’s immune system from damaging the foetus in the womb. A Swedish pathologist, Erik Larsson, has recently discovered that these syncytins are also playing some important, but as yet unknown, function in the normal human brain.
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That was absolutely fascinating. I'm enthralled. It's an amazing story of our genes which leaves me with a great sense of wonderment.
 
Moving on

I'm glad it interested you. Do you want to travel a bit further along this odyssey? Like how did the HERV-W that codes for syncytin-1 get there? And what does it all really mean?
 
the neverending story

Okay -- so how did the HERV-W that codes for syncytin-1 get into the human genome?

The answer is through a plague retrovirus that was pandemic to our primate ancestors in Africa sometime between 20 and 40 million years ago invading the primate germ line (sperm or ovum). We are watching a similar plague retrovirus invade the genome of the koalas in Australia right now. It is thought to have begun about a century ago (animals put on an island a century ago, and hence separated from the mainland koala population, are free of it). But in just a century the plague virus has infected roughly three quarters of the millions of koalas over the Western half of Australia, and soon it will be 100%. If you think about it, a plague virus transmitted through mating, has the perfect transmission strategy. Retroviruses are persistent viruses -- in other words they never leave an individual or species under natural conditions. So one infected becomes two, becomes four, becomes eight, and so on until the entire species is infected.

A lot of biologists still think that it only takes one or a few viruses to invade the germ line of the host species, when the virus will multiply within the chromosomes. But these days the real experts no longer believe this. People like Massimo Palmarini, at Glasgow, have shown how each insertion into the germ line represents an individual host infected.

Now think about this: that means that the ERVWE1 locus represents a single primate ancestor infected with the exogenous virus that became the now endogenous HERV-W. Infection in that one individual led to the successful incorporation of a single HERV-W coded locus into the great ape, and subsequently human reproduction. It means that every man and woman on Earth is connected to that single individual infected.

The koala retrovirus is definitely inserting its genome into the koala germ line consistently and increasingly, so that within a single small populations of animals there are variable numbers of virus insertions in the koala genome from say half a dozen to 50. Each viral genome is roughly 10,000 nucleotides long, so an insertion of fifty viral genomes spread randomly over the chromosomes is actually a considerable amount of new genetic information. The viral genes, and genetic control sequences, are, of course, utterly different from that of a vertebrate animal. They have followed their own very lengthy evolutionary path to this point. But the virus is also highly evolved, and conditioned by selection, to take over the control of key aspects of its host genome -- this is part of its pre-evolved infection strategy. So every viral insert into the genome has the pre-evolved potential to change things. This is quite different conceptually, and mechanistically, from the traditional concept of mutation, which results from copying errors when DNA is replicated during cell division. In effect, a genome that is invaded by such a pre-evolved viral genome now has a dual evolutionary lineage, host and viral. This is quintessential genetic symbiosis.

The human genome has been massively colonised throughout its history in this way. We contain between 30 and 50 retroviral families, and some 200 or so subgroups. All the HERV families must have originated as pandemic retroviruses that invaded the genome and very likely many if not all the subgroups. Hence our human genome has thirty times more viral DNA than DNA of vertebrate evolutionary origins.

If we look at the HERV-W alone, which is just one of the 30 to 50 families, there are 650 viral insertions scattered over the chromosomes. The genes and sequences within these insertions remain viral, within viral control structures. They can never be regarded as vertebrate captures, or the equivalent of vertebrate genes. They retain their quintessential viral nature indefinitely. So the human genome really is a symbiotic union of vertebrate and viral origins -- in symbiotic terms this is called a holobiontic genome.

This has major implications for human evolution and for the genetic basis of disease. I have just had the third paper out of five published in the J of the Royal Society of Medicine, which explains how such an inheritance can give rise to disease. This paper, which is referenced on the fprbooks website, puts forward a new way of looking at the autoimmune diseases, which affect one out of twenty people in the Western World.

I'll pause and answer questions on this if there are any.
 
Out of interest Frank, how does Cosmological background noise play into your Virolution?

I ask because I'm interested in what sort of radiation can spawn mitosis and whether a matrix of differing frequency could actually cause a spacetime distortion that could cause something similar to read-writing data in the wrong order, in regards to cellular replication.
 
getting elemental

Hi,

You ask an interesting question, but I don't think it is relevant to viral symbiosis. But looking more universally at evolution, radiation is certainly a potent cause of mutation, in the correct and original definition of mutation. Many of the great experiments done with the fruit fly used radiation to induce mutational DNA errors.

As to what impact radiation might have had in the primal environment on Earth, at the stage before cellular life when things were at the stage of self-replicators! There was no protective ozone layer -- so I think you could argue that energy radiation of various sorts would have been very considerable, and influential. You could argue that on primal words out there in the cosmos, the same influential radiation is operating. Add to that that all of complex life on Earth is ultimately depended on light radiation -- through the energy capture involved in photosynthesis.

So there is something very important in what you are saying.

One of the things that fascinates me, talking more widely about evolution, is that all of life is also dependent on soil bacteria -- and also soil insects. If either were killed off, all life on Earth (other than perhaps autotrophic bacteria) would cease. The explanation for this is the interruption of the great elemental cycles, such as carbon, nitrogen, etc.

This makes the notion of planetary colonisation rather more difficult than people might otherwise imagine. You might colonise Mars, for example, by taking what you need up there and keeping a small colony alive, but to make a green and blue Mars, or in other words a living planet, you would need to recreate the great cycles of life that we find on Earth. These evolved, Gaia fashion, over vast time periods with complex interaction between life and the inanimate aspects of the biosphere.

Hey, perhaps you have opened up a real can of worms here.

All best,

Frank
 
At what age do students begin to learn about viral genetic symbiosis nowadays? Degree level? It's totally new to me incidentally (as a non-biologist).

Also I have a question w.r.t the possible unsuspected evolutionary paths of other animals. I'm currently interested in the idea of cartilaginous rays having evolved the ability of true flight. (The cownose ray uses specialised ligaments to strengthen it's bite so that it can crush the shells of crustaceans). It seems that viral genetic symbiosis could be used to account for almost any such spurious suggestion, doesn't it?
 
getting genned up

I think the answer is that students even at graduate level are not taught viral symbiosis -- or should I say haven't been taught it until recently. In part this is because it is relatively new and in part because symbiosis itself hasn't been well taught at many universities -- though this is changing very rapidly right now and membership of the International Symbiosis Society is spiralling. Anybody is welcome to join the ISS. People who do so soon become inspired since it involves the study of whole organisms in a myriad different fascinating interactions. Symbiosis is literally everywhere and omnipresent, when you actually look for it.

I gave a keynote talk on defining viral symbiosis at a virological symposium at the Noble Foundation in Oklahoma last year and the whole session was devoted to viral symbiosis. But that was a first because the local Professor of Botanical virology, Marilyn Roossinck, has been pioneering it into plants, with some very interesting results. Her group has been looking for hitherto unknown viruses in plants -- i.e. viruses in healthy plants, hence viruses not causing disease. They appear to be screening all the plants they can lay their hands on in Costa Rica, which is a fairly extraordinary exercise. That's a first step to quantitating and qualifying what the viruses are actually doing in the plants. They had discovered several thousand in their first eighteen months, which is impressive. They had already kickstarted this by looking in their own back yard to discover, using a symbiological perspective, a virus that enabled grasses to survive in the arid ecosystem of Yellowstone Park. This virus infected a fungus which in turn infected the grasses. It was a three way symbiosis, published in Science. The evidence to date suggests that the virus probably makes a metabolite that is important to the plant survival.

I'm pleased to say that I've been contacted by several colleagues in Europe and the States who are now thinking of extending the screening of symbiotic viruses to animals (including insects).

A book I published about six years ago (Darwin's Blind Spot) has been used to teach undergraduates and graduates about viral symbiosis in about half a dozen universities, in America and Asia. Nobody other than me, to my knowledge, is interested in further research in the UK, though I have lectured quite widely here and the audiences tend to be very interested, once they grasp how simple it all is. I'm afraid it's the old story, a concept pioneered here has been quickly adopted elsewhere.

However, Sheffield Medical School introduced a new five module optional course on evolutionary biology into the final year in spring this year. I teach it together with Philip Chan, a vascular surgeon interested in evolutionary biology. So viral symbiosis is now being taught at at least one Medical School.

Publication of the five review papers (currently the first three are out) in the J of the Royal Society of Medicine is also helping to spread the word in a practical sense. Also publication of Virolution is interesting university colleagues globally. I have been busy with e-mail communications on this. So, globally, the situation is changing. I hope colleagues here in the UK do begin to develop the concept, since the research potential for biology and medicine is very great.

If you guys want me to, I shall follow this up with a medical application that might interest people.
 
P.S. a scary piece of news

As you will now know, I like a little joke, or entertainment, or both.

I've always written some fiction even while very busy in science. At the moment I am very interested in young adult fantasy, for its own sake -- it is very creative -- but also because it is what youngsters like to read. I have only ever written a single work of science fiction, which I'm told is fairly terrifying. Perhaps a reflection of my time working in plague zones.

While waiting for a reply on the more serious issue of medical applications of viral symbiosis, if you guys on this website would like to read a scary sci-fi, I would be happy to open up the entire e-book to you free of charge.

I was fascinated by the idea of the creation of a truly artificial life-form, and the evolutionary implications...

Go on... have some fun with a science fiction novel written by a scientist!

Perhaps there's some way I can make it available to you on this site in pdf format?
 
A challenge, perhaps?

So maybe I am asking a question:

Is creativity in the arts and sciences coming out of the same well?
 
Getting back to basics

Hey -- maybe this last question would initiate an interesting thread of its own irrespective of the general thread of discussion here?

I promised in asking people to look at the slightly daunting picture of the ERVWE1 locus that there was a reason I was picking on this. If you like, I shall return to this line of communication and show how a simple understanding of viral symbiosis enables us to extrapolate from there to an important line of medical research into the autoimmune diseases and particularly multiple sclerosis.

What do you feel about this?
 
A viral role in MS

Okay, I'll put together some information. I hope, since I will then have submitted the requisite 20 postings I might be allowed to include a small illustration.
 
A HERV Role in the Cause of MS?

This is a theme based on a scientific paper published in the J of the Royal Society of Medicine on October 1 2009. It develops the medical extrapolations of viral symbiosis in the evolution of the human genome that were explained in lay person terms in the book Virolution.

In 1997 French and UK workers reported an unknown retrovirus in tissues from the brain and blood cells (lymphocytes) from patients with MS. They called it the MS retrovirus, or MSRV. Later this was seen to fit the genetic signature of a human endogenous retrovirus, known as a HERV-W. For years people weren’t sure if this was an exogenous (freely infectious) retrovirus behaving in a typical infectious manner, or an endogenous virus fixed within the human chromosomes.

The typical acute pathology of MS involves discrete foci of inflammation within the brain, known as “plaques”. These show damage to myelin – the insulating material wrapped around nerve cells. The cells that lay down myelin are known as oligodendrocytes. MS is common in Sardinia and Italian researchers examining these MS patients found intense staining for the HERV-W env gene in brain cells, known for their starry shape as “astrocytes” within the plaques of patients with MS. This appears to be specific to the astrocytes within the plaques and is not found to any significant degree in normal brains or outside of the plaques in patients with MS.

Canadian colleagues then showed that a HERV-W envelope gene very much like syncytin-1 modified the immune response within the astrocytes of the acute plaques in the brain of MS patients. They also went on to demonstrate that this “syncytin-1-like” expression caused the astrocytes to make chemicals that killed local oligodendrocytes.

This clearly fitted with what was known of the pathogenesis of MS.

Even more tantalising was the discovery by the Italian researchers that patients with newly diagnosed MS had very high levels of the MS-associated retrovirus in their peripheral blood lymphocytes. And more tantalising still, the virus cleared from most patients over a three month period after starting beta-interferon therapy.

But important mysteries remained.

Why should syncytin-1, the env gene of a HERV-W long conserved by natural selection as part of our essential genetic make-up, now act as the trigger for an important auto-immune disease?

New studies, in Germany and Italy, suggest that the presence of a second HERV-W, on the X chromosome, may be inappropriately expressed in patients with MS. The env gene of this HERV had been switched off by natural selection (a “stop” codon) during human evolution. It is possible that we are witnessing the unstopping of this gene by HERV-to-HERV recombination (an essentially symbiotic evolutionary mechanism) within the tissues of MS patients.

Important questions remain to be resolved, but these issues are now being further investigated.

In other words we can assemble the jigsaw of results from leading investigators in four or five different research centres to conclude that the env gene of a HERV-W endogenous retrovirus is likely to be playing an important role in the pathology of MS.

Further research is needed to determine if the causative gene really is syncytin-1, the env gene of the well-known virus on chromosome 7, or whether the pathology is triggered by the second env sequence, possibly through recombination of HERVs that has “unstopped” the action of natural selection on the HERV-W on the X chromosome.

How might a symbiotic perspective introduce an additional possibility?

Work by scientists in many centres has shown that HERVs are expressed in the normal human brain. Research as yet to be published in Sweden has also shown that syntycin-1 is densely expressed in the normal human brain – in other words it is fulfilling an unknown, but important function, or functions, in normal brain physiology. Based on this, and an understanding of viral symbiosis in human evolution, it is also possible that expression of a normally suppressed HERV-W env gene on chromosome X in MS patients is dysregulating a symbiotic immunoregulatory function of syncytin-1 within the astrocytes.
 
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Frank Ryan said:
How might a symbiotic perspective introduce an additional possibility?

Work by scientists in many centres has shown that HERVs are expressed in the normal human brain. Research as yet to be published in Sweden has also shown that syntycin-1 is densely expressed in the normal human brain – in other words it is fulfilling an unknown, but important function, or functions, in normal brain physiology. Based on this, and an understanding of viral symbiosis in human evolution, it is also possible that expression of a normally suppressed HERV-W env gene on chromosome X in MS patients is dysregulating a symbiotic immunoregulatory function of syncytin-1 within the astrocytes.
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Yes, I see how important a complete understanding really is for the eradication of viral diseases. This work is monumental in the progression of humanity. It's a shame it isn't getting more local recognition and attention.
 
things happening

Not to worry -- things are actually progressing very well. The Royal Society of Medicine and the Linnean Society of London have both been very supportive here in the UK, as are increasing numbers of medical colleagues here and globally. This morning alone I have had e-mails expressing support and interest from virological and evolutionary colleagues in America, Poland, France and Australia -- so I hardly have cause for complaint. An idea as revolutionary as this takes time to percolate through.

My continuing purpose, as laid out in Virolution, is to help bring the two worlds of symbiology and virology together. And the main way to achieve this is through careful definition and education, together with reassurance that the new ideas don't clash with the old, meanwhile assisting people to set up pioneering research in biology and medicine.

In essence my contributing to this website is part of this same educational exercise. I'm glad you found it interesting.
 
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