THERE was a recent article in NewScientist suggesting that viruses are the unsung heroes of evolution. Whilst that is somewhat of a sensationalist position, there is a great degree of truth in it. Many anti-evolutionists seem convinced that it is mathematically impossible that genetic variation and mutation can be a sufficient substrate upon which natural selection can act.
What they forget is that whilst a mathematical proof is always the truth, it is a truth that is dependent upon whether the mathematical model accurately reflects the physical problem. Mathematics is limited to the validity of the assumptions that underpin the statement of the problem, thus in the fixing of certain variables it’s important to distinguish between getting the maths right and getting the problem right.
The variation seen in a species, upon which natural selection can act given circumstances that favour one variation over another, is encoded by alleles; this is the name given to different “versions” of the same gene, thus for eye colour, different alleles may be: brown, blue, green etc. Some alleles are dominant, some are recessive; the dominant ones win and get used, the recessive ones lose and don’t get used. The dominant and recessive alleles are both part of your genetic make up, and this is called your genotype. The dominant alleles result in a physical attributes in the organism, such as brown eyes, and these physical attributes are known as the phenotype.
It is true to say that whilst all phenotype is derived from the genotype, not all genotype results in phenotype. Dominant traits, because they are aspects of the genotype that are reflected in the phenotype, are traits that can be acted upon by natural selection; however recessive traits are effectively hidden from natural selection unless the DNA that codes for the recessive alleles is physically linked to a piece of DNA that results in some other dominant trait that can be selected for or against. This recessivity maintains a store of genetic diversity.
What has this got to do with viruses? Well, viruses are also a source of new, and potentially hidden, alleles. Viruses can invade your cells, and upon invasion they have two choices, depending on the type of virus: when the going is good, they can use your cells to manufacture new virus, compromising those cells or more often resulting in the cell’s death, or they can insert themselves into the host genome and wait for more favourable conditions under which to replicate themselves.
The interesting thing is that viruses have been doing this to organisms for billions of years, and the number of viral particles out there in the environment is sufficient that we can think of all cellular organisms as bathing in a sea of virus particles and viral DNA; thus the insertion of their genetic information into various hosts over history has been a most significant for of acquired genetic traits, often referred to as horizontal gene transfer.
What is even more startling is that these acquired genetic traits can be inherited, i.e. even though they inserted into an adult organism, the adult organism can pass them on in their genes to progeny. This is almost Lamarckist in principle, though of course I’m not suggesting that we resurrect Lamarck‘s position.
Here are two examples:
Human Herpes Virus VI can be passed from adult humans to their children, not via infection of the foetus in the womb, as might be expected, but through integration into adult chromosomes. It is safe to say that if one virus is doing this, there are probably considerably more doing so, which we’ve yet to identify. So right here you have additional sources of genetic variability, because viral proteins can be co-opted for host functions if they’re in the right place at the right time.
One reported Human protein that is derived from a viral source, thus seems to have been co-opted in this manner and is now an integral part of our genetic make up, is Syncytin. Syncytin started life as a gene encoding a protein in the viral envelope of a human endogenous retrovirus, HERV-W (a retrovirus being one of those viruses that can write themseves into their host’s genome). In Humans it now performs a function in the development of the placenta.
The subject of my PhD was essentially horizontal genetic transfer in bacteria, the like of which leads to the sudden ability of recipients of such genetic transfer to resist antibiotics/disinfectants/heavy metals or be able to metabolise chemicals for food that they couldn’t before. Bacteria are therefore not only able to become resistant to an antibiotic spontaneously, but can also acquire the ability ready-made and packaged.
I think it safe to say that the occurance of horizontal genetic transfer in all organisms, bacteria, protozoa, plant, fungi and animals throughout evolution has been a major player in the devlopment of organisms in the great kingdoms of life. Thus whilst we can demonstrate that mutation is sufficient to generate variabilty upon which natural slection can act, there is a whole other source of genetic variability that is a very big cherry on the already well iced cake.