By John Pickard
I came by this book, Virolution, by Frank Ryan, as a Christmas present, from someone who knew my background and interest in Science. In the light of the coronavirus pandemic, it was moved forward in my ‘reading queue’ and has proved to be a very interesting read.
The book is not an easy read for non-scientists, particularly its later chapters, but it raises some extremely interesting points and the author suggest that viruses may be linked to sudden jumps in the evolutionary development of plants and animals, including humans.
Switching genes on and off
It is probably useful at first to give an overview about the mechanisms of inheritance and about how viruses work. It is common knowledge that inheritance is coded in a complex molecule, DNA, which is found in all living cells. DNA is organised into large structures called chromosomes and all human cells have 23 matching pairs, ie 46, with other organisms having different numbers. Each one of a ‘pair’ is not quite identical because one has come from each parent.
Sections of a chromosome, called ‘genes’, are responsible for the inheritance of all an organism’s features like appearance and shape, but also for more ‘hidden’ features to do with internal metabolism, like digestion and respiration.
Every cell in the human body has an identical set of genes. What is still unknown to genetics – and is at the forefront of a lot of modern research – is why and how some genes are switched off and others are switched on in a cell. The switching has to happen, otherwise every cell would be identical and there would not be different liver, muscle, nerve, kidney, skin and other cells. For a cell to be able to do its job as part of some particular tissue, only some of its genes have to function and the rest need to be switched off. Thus, certain genes are “expressed” (ie switched on) and if the switching mechanism fails, it can cause cancers and congenital conditions.
Humans: 20,000 genes in the genome
In practice, genes rarely work individually, but interact with others, so by means of genes, or complexes of genes, characteristics are inherited from generation to generation. Humans have about 20,000 genes. All organisms are said to have a genome, which is the sum of its genetic structures.
If a particular gene can impart a useful ‘value’ to a living organism – a feature that improves the likelihood of it being able to procreate in its given environment – then that feature and the gene responsible for it are passed down the generations.
Richard Dawkins coined the expression the Selfish Gene, as an illustration of how genes are selected by nature to survive, because the characteristic they impart is selected. The term was a literary device – Dawkins did not suggest that genes had ‘thoughts’ or ‘intentions’. But he explained that for a gene to be perpetuated down the generations, it must impart some advantage to its ‘host’ organism. It is as if genes ‘want’ to survive.
Bacteria different to viruses
Coming to viruses, we need to distinguish them from bacteria, which are living cells and which often function in isolation from other cells and organisms. Viruses are a lot smaller than bacteria, but their key difference is that they cannot ‘function’ on their own behalf.
Outside of any other cells, viruses are completely inert and individual viruses are referred to as virus particles. A virus particle is rather like a ‘packet’ of DNA (or a related molecule, RNA) surrounded by a protective protein coat. Its precise shape and structure depend on the type of virus, but all of them follow the same pattern.
On its own, unlike a bacterial cell, a virus particle cannot engage in any metabolic activity. It just ‘sits’ there, as it were, doing nothing. It is for that reason that there are arguments about whether a virus is really ‘alive’ in the same way as other living organisms. Viruses only come ‘alive’ inside ‘host’ cells. They can only reproduce inside living cells, including, by the way, bacteria.
Viruses are all around us
There are a lot of viruses, inside us, on us and all around us and an uncountable number of different types. According to the virology website “If we assume that the 62,305 known vertebrate species each harbour 58 viruses, the number of unknown viruses rises to 3,613,690…if we include the 1,740,330 known species of vertebrates, invertebrates, plants, lichens, mushrooms, and brown algae. This number does not include viruses of bacteria, archaea, and other single-celled organisms. Considering that there are virus particles in the oceans – mostly bacteriophages – the number is likely to be substantially higher”. 1031 for the non-mathematicians, is a 1, followed by 31 zeros. A lot of viruses. Scientists have even been successful in extracting viruses from frozen tissue collections and in extracting DNA from fossil organisms
At least one virus can be created from scratch
Viruses are classified according to things like their shape, their preferred ‘hosts’ and their genetic make-up. One type of viruses are the “retroviruses” so-called because of the way they ‘capture’ and manipulate host DNA…more of which later.
Some viruses are very simple. “If you know the genetic formula of a virus,” Ryan, explains in Virolution, “you can reconstruct it” and in fact, he gives the chemical formula of a polio virus as follows:
C332,652H492,388N98,245O131,196P7,501S2,340
It was as long ago as 2002, he points out, that a scientist in New York became the first person to reconstruct the polio virus “from mail order components back in his lab.”
Once a plant or animal cell is successfully invaded, the virus particle releases its own DNA into the cell, to effectively take over the DNA of the cell and therefore the management of its metabolism. Instead of continuing its ‘normal’ functions, the cell is commandeered to making millions of copies of the virus particle, which are then released to infect other cells. Eventually, the host cell dies, by which time, not only has it failed its host by not carrying on its proper function, but it has released millions more viruses to infect other cells.
No advantage in killing the host
Because of their capacity to commandeer and manage the host DNA, viruses can mutate extremely rapidly, much more so than other organisms. Using the Dawkins ‘selfish gene’ metaphor, we can imagine a virus particle ‘wanting’ to be modified so as to be more successful in passing on its genes.
In relation to coronavirus, or any virus, therefore, there is no evolutionary ‘advantage’ in killing its host. For its own genes to survive and be procreated, it is far better for a virus to mutate towards being more infective, but less dangerous to its hosts.
According to the early reports of different coronavirus strains, that is indeed what seems to have happened, with the later strains being more easily transmitted but less dangerous than the first.
Now we come to the interesting part and the focus of Frank Ryan’s book: the suggestion, in effect, that viruses have played a key part in evolution, especially where there have been significant and rapid ‘jumps’ in evolutionary change. He argues that “Analysis thus far has shown a very tight correlation between the evolutionary tree that illustrates the history of the mammalian host and the evolutionary tree that illustrates the history of viruses…” Ryan’s book links human DNA (and other organisms, but we’ll stick to humans) directly to viral DNA. “What if both the virus and its mammalian host,” he asks, “are influencing one another’s evolution, one evolutionary tree, interacting with the other, over the vast time periods of their co-evolution?”
Right out of Dialectics of Nature
In a passage that could have come right out of a modern-day equivalent of Engels’ Dialectics of Nature, he challenges the idea of a species being separate at all. He suggests that “terrestrial life is a dense web of genetic interactions”.
In fact, it is already well known that humans are in a close symbiotic relationship with billions of bacteria in the gut. For every single ‘human’ cell walking around in a ‘person’, there are ten bacterial cells in the gut. The human microbiome is another part of cutting-edge medical research and it is now realised that an unbalanced microbiome can lead to many form of ill-health.
But Frank Ryan takes this a whole step further. “…is it possible”, he asks, “a virus could have a beneficial effect on an animal species…if the presence of a virus might help a host survive?”. Ryan, along with other virologists, now talk about that branch of biology that looks specifically at symbiotic relationships as symbiology.
Ryan offers a mechanism whereby a virus can play a role in influencing the evolution of the host. The process begins with an “aggressive infection” by an exogenous (ie “outside”) retrovirus, often from a closely related or similar species. That infection might ‘cull’ large numbers of the host species, perhaps the big majority, but over a period of time two things happen. Firstly, a fraction of the host species with an in-built genetic immunity will survive and thrive, eventually to become the main population. Secondly, the virus itself will mutate in such a way that it becomes less lethal to the host and is therefore more likely to be passed on…think ‘selfish’ gene. At this end point, the virus is no longer an aggressive invader but an endogenous and harmless virus, living perpetually inside the host. Exogenous has become endogenous.
Most of our DNA was thought to be ‘junk’
There is ample evidence for this process taking place across many species, but no less so than in human DNA. Looking at all the DNA in a normal human cell, there are no more than 20,000 genes and much of the chromosomes are composed of what used to be called ‘junk’ (ie useless) DNA. Science has now discovered, and in relatively recent years, that, as Ryan says, “the vertebrate component of our genome – the part we normally associated with what makes us human – amounted to a mere 1.5% of the whole.”
But Science is beginning to realise that what used to be considered ‘junk’ is far from it. Large sections of human DNA are identical to sequences of DNA found in retroviruses. In fact, although it is part of the ‘human’ makeup, these are now referred to as the HERV sections – Human Endogenous RetroVirus – of the human genome. “Today we recognise that our retroviral legacy is made up of vast numbers of copies of human endogenous retroviruses…”
Virus gains a kind of ‘immortality’
It is as if a virus has found the perfect way of continuing its own genes, by completely incorporating them in the host genome. This process, Ryan explains, “involves the exogenous virus giving up its freedom for longevity, perhaps a kind of immortality, as a component part of a new genome”. The evolution of the host, therefore, is not just the evolution of the original species genome, but a co-evolution of a new, combined genome.
In relation to the human species, Ryan suggests, the evidence is that the majority of the HERV elements in our DNA were incorporated 10 million years ago in our evolution, during a stage of primate evolution. But there are also important sections believed to have more recent origins. This is not the time or place to discuss the complexities and ramifications of human evolution, but a viral modification of genes is certainly a plausible mechanism for sudden accelerations in evolution at any point. Selection may be the ultimate arbiter but given selection pressure on a species in a given environment and location, a viral alteration of important genes may have a sudden and dramatic affect.
Strong argument put forward
What genes would be affected by such an evolutionary “lightning strike” as it is put in the book? Going back to the unknown mechanisms that turn genes on and off, Ryan puts forward a strong argument suggesting that as much as 34% of the human genome are “retroviral derived or controlled.” That word ‘controlled’ is important. He cites instances where it is known that HERV elements in the genome are active in gene control (‘switching’) and it is in that whole area of modern genetic research that HERV elements are being looked at. Thus, a dialectical approach to evolution – where long periods of relative stability are interrupted by sudden and rapid leaps forward – is given a genetic mechanism to account for it.
There are other important elements in the book that look at mechanisms of evolution outside of the mutation-selection model of traditional Darwinism. Readers will have to find these themselves in the book. Suffice to say that at the end of the process the success or otherwise of evolutionary modifications still depend on natural selection – does the new, changed organism have a greater or a lesser chance of successful procreation in the given natural conditions?
The human microbiome is now a well-known feature of medical research and even in treatment today. Ryan’s book opens a door to another particularly important element of the microbiome and one that is normally overlooked: that part of the microbiome that is viral…and at the same time a part of us. Well worth the read.
April 30, 2020
