Viruses Are The Ultimate Symbionts

[Ophiolite]

I would like to start with the genetic locus known as ERVWE1, which is essentially the genome of a HERV-W (human endogenous retrovirus W) whose env gene codes for the protein syncytin-1, which is essential for normal human placentation.

While it is essential for normal human placentation as it currently exists am I correct in assuming that placenta formation would still occur in the absence of this protein, it is just that its character would be different? If so do you think this difference would have any significant impact on the nature of a developed human?
(Please note I am not disputing that the presence of this protein represents an evolutionary step, I am just interested in whether or not it is an important evolutionary step.)

 

[Walter L. Wagner]

Glad you survived the Canaries!

It's fascinating that what you seem to suggest is that different mammalian lines 'suffered' different retrovirus infections, conferring a benefit to that line in placental linings, after the retroviri became incorporated into the host DNA and its descendants.

As per Ophiolite above, how does that benefit work - i.e. how important was it in developing primate lineages? What does it do?

 

[common_sense_seeker]

When you look a little more broadly you realise that the differences of opinion between disciplines are often due to that blinkering of vision brought about by super-specialisation.

Hah! There would appear to be room out there for some of us to deliberately flout the tendency and become generalists.

Frank, I have a couple of questions for you:

Q1: If a particular species of animal has a higher number of parasites than average, and parasites carry a high number of viruses, is it reasonable to suggest that this species is more likely to be subject to 'advanced' evolution via viral genetic symbiosis? (P.S does the maxim 'what doesn't kill you makes you stronger' apply?)

Q2: When do you think Davd Attenborough will be presenting a TV 'Life On Earth Virolution Special'?? Will it take a few years before the BBC natural sciences catches on?

 

[Frank Ryan]

viruses and the tree of life

The subject of viral symbiosis appears to be becoming topical. That wasn't the case for the first decade or so of my working in it, but things have changed. We needed to get into the age of genome decipherment to realize just how paradoxical and extraordinary the structures of genomes, universally, really do appear to be, and how major the components generated by viruses.

Recently Moreira and Lopez Garcia wrote a paper in Nature Microbiology Reviews in which they claimed that viruses have no place in the tree of life. I think they are very much mistaken. Villarreal and Witzany have just written a rebuttal which is available free on-line. See Villarreal,L.P.,Witzany,G.,Virusesareessentialagentswithintherootsandstemofthetreeoflife.J.Theor. Biol. (2009),doi:10.1016/j.jtbi.2009.10.014

It has become increasingly evident that viruses have been contributing, in a major way, to life from its beginning to all life forms within the present biosphere. That they should have done so might appear somewhat shocking at first glance, but when you consider what viruses do as part of their normal life cycles (I get criticized for calling them that but that is exactly what they are), the extraordinary intimacy of the virus-host relationship (you can't get much more intimate the germ-line union), and the power they have for genetic and genomic manipulation of their hosts, their ability to modulate host immunity, and so on, you realize why I put the heading on this thread that viruses are the ultimate symbionts.

If you have trouble accessing this paper let me know and I'll send it by regular e-mail as a pdf attachment.

Now if you examine the ERVWE1 locus, can you suggest any alternative evolutionary mechanism for such a locus within the human genome other than genetic symbiogenesis through genomic union. The key gene is viral, it is within a viral genome, it is promoted by the viral 5' LTR, further regulated by a second viral LTR. The vertebrate bits interest me, for example the intron between the 5' LTR and the first viral gene -- is this important to the symbiogenetic function of the syncytin-coding gene for example? Is this a zone of interaction between viral and vertebrate lineages?

With regard to the questions about placentation, Massimo Palmarini thinks that placentas evolved in simple form without viruses and were then further improved by viruses. But Luis Villarreal thinks the opposite. But this is a question that can be answered with more work in marsupials.

One thing is for sure. Without the viral contribution the human placenta would be a much poorer, and less efficient organ. If you think about it, the maternal products have to cross through cytoplasm to get to the fetus, since there are no cell boundaries they could pass through. This introduces the potential of high quality monitoring and control. And just below the fused layer, there is a second layer of trophoblasts that are thought to be differentiated by syncytin-2 to prevent maternal rejection of the foetus. Now add to this the six more viruses we currently know of that are active in the placenta, playing roles in hypertension of pregnancy, maybe others stress-responsive. The mind boggles at the full story of viral symbiosis here, though much remains to be understood.

I've just heard from Erik Larsson that they have looked again at the role of viruses in the normal human brain. I gather their new studies confirm and extend what I wrote about in Virolution. I just can't wait to read the published data when it appears.

Meanwhile, an international organization is interested in a conference on such themes next year, or possibly the year after. They are offering help with funding and organization. It's early days but it if happens it might prove very interesting.

 

[Frank Ryan]

further comment, not reply

Hi my friend,

First -- I should have said "Good to be back!" Although the weather here is on the turn for the worst.

Now as to specific answers to your questions:

Q1: If a particular species of animal has a higher number of parasites than average, and parasites carry a high number of viruses, is it reasonable to suggest that this species is more likely to be subject to 'advanced' evolution via viral genetic symbiosis? (P.S does the maxim 'what doesn't kill you makes you stronger' apply?)

F: I don't think the viral load within the genome will depend on exogenous parasites, only on the species' past evolutionary history, and, ironically, on the number of retroviral (or the equivalent in other kingdoms) pandemics the species has suffered. There probably is a germ of truth in the maxim, if can get away with the joke. I can't say that every pandemic inserts into the germ line but it would appear that a lot do, and they do so with effortless ease, judging from the koala experience. But I can say, without any real doubt, that the quantity of viral insertion is important, and probably the variety of endogenous families, is also likely to be important. So that's a very good question that nobody has asked me before.

Q2: When do you think Davd Attenborough will be presenting a TV 'Life On Earth Virolution Special'?? Will it take a few years before the BBC natural sciences catches on?

I don't think that Attenborough will ever look at viruses. But I could be wrong. I like his programs although I often wonder who, out there, has really done all the background work, since no one biologist could be so expert across all disciplines.

 

[common_sense_seeker]

Q1: If a particular species of animal has a higher number of parasites than average, and parasites carry a high number of viruses, is it reasonable to suggest that this species is more likely to be subject to 'advanced' evolution via viral genetic symbiosis? (P.S does the maxim 'what doesn't kill you makes you stronger' apply?)

F: I don't think the viral load within the genome will depend on exogenous parasites, only on the species' past evolutionary history, and, ironically, on the number of retroviral (or the equivalent in other kingdoms) pandemics the species has suffered. There probably is a germ of truth in the maxim, if can get away with the joke. I can't say that every pandemic inserts into the germ line but it would appear that a lot do, and they do so with effortless ease, judging from the koala experience. But I can say, without any real doubt, that the quantity of viral insertion is important, and probably the variety of endogenous families, is also likely to be important. So that's a very good question that nobody has asked me before.

Thanks for the explanation Frank. I'll take that as meaning that although not necessarily a direct link, one might expect a tendency of some sort with regard to what I'm proposing.

I have another question or two:

Q1: What does the animal tree of life look like? There's an interesting debate in Science Illustrated this month. Here's a sciencemag article on the subject: No Sponge In Human Family Tree: Sponges Descended From Unique Ancestor.

Current model - simple animals came first
New model - complex animals evolved separately?

How would the new model fit with the ideas of virolution compared to the standard model? Would there be any difference? Could virolution provide a mechanism or 'fingerprint' to solve which picture is the correct one?

Q2: Could virolution be a new way of identifying the definition of exactly what a species is?

 

[Idle Mind]

Thanks for the explanation Frank. I'll take that as meaning that although not necessarily a direct link, one might expect a tendency of some sort with regard to what I'm proposing.

No, that's not a reasonable interpretation of his answer. You make some pretty bold assumptions that you haven't shown to be true. Why do you think parasites carry a higher number of viruses? And given that viral infections are pretty species-specific, why would you assume that a species that carries a higher number of parasites would then be subjected to the viral load of the parasite itself?

 

[common_sense_seeker]

No, that's not a reasonable interpretation of his answer. You make some pretty bold assumptions that you haven't shown to be true. Why do you think parasites carry a higher number of viruses? And given that viral infections are pretty species-specific, why would you assume that a species that carries a higher number of parasites would then be subjected to the viral load of the parasite itself?

It was a comment based on my knowledge of statistics, that's all. It was a gross generalisation I admit, but with a statistical germ of truth, was it not?

 

[Idle Mind]

No, not when considering viruses as a driving factor for mutation and thus evolution.

Can you provide a source for the statistics showing that organisms that are more highly affected with parasites have a higher incidence of viral infection? Or one that shows that parasitic organisms carry a higher viral load than other, non-parasitic organisms?

 

[common_sense_seeker]

No, not when considering viruses as a driving factor for mutation and thus evolution.

Can you provide a source for the statistics showing that organisms that are more highly affected with parasites have a higher incidence of viral infection? Or one that shows that parasitic organisms carry a higher viral load than other, non-parasitic organisms?

It was purely a layman's interpretation.

 

[Ophiolite]

It was purely a layman's interpretation.

You omitted the mis in front of interpretation. Now please go away and stop fouling yet another thread with your stupidity.

 

[Frank Ryan]

learning about host evolution from viruses

Our knowledge of the role of symbiotic viruses in host evolution is still at a very early stage, but I think I am not being presumptuous when I say that the evidence is pointing to a very major role. I am still waiting for my Swedish colleagues to publish their findings on the role of the two syncytins in the normal human brain. I have had the opportunity of seeing their immunological stains, and they are very dramatic. I gather they have repeated the stains using different techniques just to be absolutely sure the dramatic finds are representative, and, I am led to believe, have confirmed them. When published, they will represent the next big step from the rapidly expanding work on the eight different viruses involved in placentation.

In fact five or six different human endogenous retroviruses are now being reported by several different workers in normal brains. HERVs have been associated with every known autoimmune disease (as far as I know) and all forms of cancer. But we are hampered by a lack of understanding of their normal physiological roles. This demands further investigation. I am planning a couple of Quo Vadis papers to help biologists and medical geneticists to plan how to take the theory forward in practice and apply it to disease. I am also writing a feature article for New Scientist that will help spread the word.

There has been quite a big reaction, globally, from scientists to publication of Virolution, which has surprised me. The book was intended for a lay readership and I expected to hear more from scientists re the accompanying papers, but now it proves nearly always to be the book that provokes their interest. One interesting thing to come from it is the likelihood of an international conference where various related themes, with inferences for health and ecology/ biodiversity/ environment, etc, will feature. I think this is likely to happen because two potential sponsors have already entered the arena. These days it is so difficult to get any sponsorship for science, this is unusual, and particularly so when they approach me rather than the other way round. I have also made contact with likely speakers, again with a very enthusiastic response. So it is looking rather positive for 2011. More anon.

Returning to how viruses can tell us things about host evolution, one very interesting aspect has come from Massimo Palmarini's research. He believes that each ERV insert in host chromosomes represents an individual ancestor infected. This contradicts the earlier belief that HERVs were mobile within genomes (they are still included with LINEs and SINEs as retrotransposons). If Palmarini is right, and the evidence from the current koala epidemic suggest that he is, then we might be able to deduce evolutionary events, and timing, from the patterns of the vast numbers of different insertions in host animals. In sheep Palmarini, and a vast host of co-authors, have produced a beautiful paper dating the origins of domesticated sheep from viral insertion patterns.