Or are they parts of the genome which cause diversity?
by Matthew Cserhati @ Creation Ministries International.
Published: 14 January 2020 (GMT+10)
Prefaced and Corrected by Barry Desborough, author of The ERV FAQ @ Endogenous Retroviruses - Frequently Asked Questions
8 April 2020
Preface
Endogenous retroviruses (ERVs) provide some of the most powerful evidence for common descent between different kinds of creatures because they are genetic “signatures”, written by retroviruses mostly into the genomes of our common ancestors. Creationists try desperately to cast doubt on this conclusion, by questioning whether ERVs do actually derive from retroviral integrations into our DNA. The koala retrovirus, (KoRV) presents them with a huge problem, because here is a virus that is in the process of becoming endogenous. See The Koala's Tale. There follows a creationist attempt at firefighting this problem. My corrections and comments are in red.
Does some of our DNA really come from viruses?
Some evolutionists geneticists and virologists allege have found that 8% of the human genome originated from viruses. This number is ambiguous, since different authors include different genetic elements as viruses, such as SINEs and LINEs. For example, Alu elements make up at least 11% of the human genome.
According to another study, 22.4% of the genome is covered by endogenous retroviruses (ERVs). No. the usual figure quoted is around 8%.
They claim find that this came about when viruses infected humans and inserted their DNA into the human genome. This process is believed found to have taken place over millions of years of evolutionary time. However, this has never been scientifically proven by direct observation. Except by the direct observation of the sequenced genomes themselves, and by comparing them with those of other species.
Researchers from the University of Massachusetts Medical School have been studying the spread of a koala retrovirus (KoRV) as it infects the genomes of koalas from northern to southern Australia. Based on this, and a lot more evidence besides, these researchers claim that a similar process could must have also happened with other viruses in our own genome in the distant evolutionary past.
But how do retroviruses such as KoRV manage to insert themselves in the genome of a species? A retrovirus is a special kind of virus that inserts its own genome into the DNA of a host organism. Hence the ‘retro’ in retrovirus. A well-known example of a retrovirus is HIV, which infects our immune cells. Usually, retroviruses spread horizontally, from individual to individual, sometimes causing illness as they go along. But this process does not allow them to insert themselves permanently as part of the genetic material of a given species. What researchers want to see is whether the virus can transmit itself vertically, from parent to offspring. This would mean that the virus has become a permanent part of the genome of the species and will persist in the species in the long run.
During horizontal transfer, viruses spread between the body cells of two individuals. But during vertical transfer, viruses jump from a somatic cell (a regular body cell) to the germline. Actually, retroviruses integrate directly with DNA of gametes just as they integrate with the DNA of somatic cells.The germline is made up of the reproductive cells, sperm and eggs. If viral DNA is incorporated into the genome of the cells that give rise to the sperm or egg cells, then the virus provirus will survive to spread in may be inherited by following generations.
If the presence of the KoRV in the koala genome is so advantageous to koalas, then they shouldn’t be falling victim to natural selection by such debilitating illnesses such as cancer.
Um - nobody claims that KoRV is advantageous to koalas!
What do viruses allegedly do once inside the genome?
Those viruses which have become totally fixed* within the genome after a long time heritable are called endogenous retroviruses (ERVs). According to evolutionary theory, basic virology and molecular biology, in this manner, the genome would be much like a molecular fossil graveyard. In this graveyard we would find the remains of different kinds of retroviruses, as a sort of genetic ‘fossil record’ of infections by retroviruses over millions of years. The older the retrovirus, the more copies it has in the host genome, since it infected the genome much longer ago—or so the story goes. The older the ERV, the more likely it is to have become derelict, other than useful bits and bobs that are maintained by purifying selection. In the case of KoRv, we have huge numbers of ERVs in various loci in various individuals. This is compatible with a recent invasion of the koala genome.
*When we talk about genetics becoming ‘fixed’, we mean that the particular genetic pattern has become ubiquitous - present in the genomes of all individuals in a species. ERVs do not necessarily become fixed in a population. They may be present in some individuals but not others. Indeed, they may spread through a subsection of the population, and then be lost entirely. IOW, they can become extinct.
This is how evolutionists try to virologists and geneticists explain the presence of 30–40 different families of ‘viruses’ ERVs present in 1–1,000 copies each, allegedly introduced over the past 30 million years (according to the evolutionary timescale) in the human genome.
Once inside the human genome, several things can happen to retroviruses. Usually they can lose their function and degenerate into functionless DNA. They can also cause illnesses, such as cancer. This happens when the retrovirus disrupts a gene by inserting itself right in the middle of it. This would be like inserting a long paragraph in Russian into the middle of an English novel. The result would be unreadable. Evolutionists Biologists amazingly claim find that parts of retroviruses can also be re- programmed exapted or repurposed to take part in cellular processes. One frequently cited example is are the syncytin genes, which allegedly evidently originated from a retroviruses, and which was were re-coded exapted to take part in the fusion of certain cells to form part of the placenta.
How does the koala retrovirus spread?
The KoRV has been spreading over the past 100 years in Australia, according to evolutionists the evidence. In the north, koalas all have copies of the KoRV in their genome, whereas a small number in the south do not. It is interesting to note that KoRV causes lymphomas in infected koalas. Besides this, KoRV suppresses the koalas’ immune system, making them susceptible to infectious diseases, such as chlamydiosis.
Contrary to evolutionary theory, the previously described process is one major roadblock for viruses to integrate into the host genome. If the presence of the KoRV in the koala genome is so advantageous to koalas, then they shouldn’t be falling victim to natural selection by such debilitating illnesses such as cancer. Nobody claims that KoRV is advantageous to koalas. I don’t know how Cserharti gets this idea, other than from the smelly end of his alimentary canal. KoRv was discovered when it was realised that koalas were dying of a cancer in greater and greater numbers.
But there is yet a second major obstacle for the virus to fully integrate into the host genome. Like the cellular immune system, the genome has a way of dealing with these disruptive retroviral invaders. The immune system can distinguish its own cells from that of viruses, bacteria or other invaders. This kind of immune response is also present in the genome at a molecular level. On a genetic level the genome is capable of distinguishing between its own genes and the genes of viruses (such as KoRV) and bacteria. This is possible, since the structure of virus genes is different from those of koala.
The above paragraph is utter garbage. Cserharti offers nothing to back this up. Viruses are past masters at evading the immune system (in the case of HIV, subverting it) and getting the cell to replicate them. If they weren’t, there would be no viruses!
The genes of eukaryotes such as human or koala are more complex than those of bacteria or viruses. Eukaryotic genes (as in koalas and humans) are made up of several units (called exons, which are interspersed with segments of DNA called introns) which can be cut and pasted in different combinations (i.e. spliced) into a nal mRNA product to specify a protein.
On the other hand, the genes of bacteria and viruses are made up of one single unit, and are not spliced. Wrong, but irrelevant.
The KoRV genome is made up of three genes, gag, pol and env, the last of which codes for the protein envelope of the virus (see g. 3). Of these, the gag and pol genes are prokaryotic, and are not spliced as the eukaryotic genes, whereas the env gene is. To deactivate the gag and pol genes of KoRV, the koala cell produces so-called piRNA molecules. The piRNA sequence is a complement of the gag and pol genes. The gag and pol mRNA and the piRNA are all single stranded, meaning they form a single helix. When piRNA binds to either the gag or pol gene, they then form a double helix. In this way the viral RNA is deactivated. Interestingly, piRNA is enriched in host tissues such as the testis, right where the retrovirus needs to insert itself into the germline.
So are you saying that there are no KoRV proviruses in any koala cells, neither somatic cells nor gametes? Did you read that back to yourself before publishing?
Does viral invasion of host genomes make sense?
The evolutionary scientific picture of viruses invading the genomes of animal species and slowly integrating as functional occasionally functional sub-units into their host’s genome over millions of years runs into numerous problems. First, The spread of KoRV within koalas has been happening for only 100 years, not millions of years. This timeframe better suits the literalist Ussherian biblical timeline rather than the evolutionary scientifically accepted timescale. It takes virtually no time at all for a virus to infect a host organism, and little time for the virus to spread through a population. Who on earth thinks it takes deep time for this process to occur? This is just false nonsense.
Second, if KoRV is useful in the long run, then why does it cause such debilitating diseases such as cancer? The researchers studying the KoRV have even suggested producing a vaccine against the retrovirus to save the koalas from extinction.
Who on earth claims that KoRV is “useful”?
How is it that so many inactive copies of KoRV survive in the koala genome? Around 8% or more of the human genome is made of retroviruses. If the KoRV is retained in the koala genome as junk DNA, it would most likely have been removed from the genome. How? It would cost the cell much too much energy and material to keep the junk DNA intact for an indefinite length of time. This would be like printing a book with extra pages of gibberish at the end over and over again. It would be superfuous to keep junk DNA in the genome for such a long period of time without eliminating it. It is much more likely that ERVs such as KoRV already had some function in the genome to begin with.
There is no mechanism known in biology to remove superfluous DNA that is neutral in its fitness effect. Cserhati fails to support his assertion that there is a deleterious cost to removing neutral genetic material. Indeed, natural selection is largely driven by the accumulation of a large variety of neutral mutations that may become advantageous when environmental conditions change. He also fails to support his assertion that “KoRV already had some function in the genome to begin with”, in the same article that falsely sneers at “evolutionists” for saying it is beneficial! It is not.
Also, it is a wide stretch of the imagination to say that retroviruses can contribute to a new function within the genome. If viral DNA is inserted at random into the genome, it is much more likely to disrupt existing genes. A blindfolded painter will most likely mess up the painting he is working on by just applying random brushstrokes to it.
Heritable changes can be neutral, detrimental or advantageous. While advantageous changes are the rarest, they contribute to the likelihood of being replicated. This is what is meant by “advantageous”. Thus, advantageous changes tend to increase in frequency in a population, while deleterious ones tend to get - er - deleted. This is the basic natural selection of heritable variations that led Huxley when he first heard of it to declare, “How stupid not to have thought of that!” It seems that creationists have never heard of it either, despite it having been common knowledge among educated people for over 150 years.
Lastly, why is it that host piRNA already exists in the genome with a sequence which is complementary to that of the gag and pol genes? It is as if the host genome had been able to look ahead and had already come up with the piRNA sequence in order to counteract and deactivate the gag and pol genes of the invading retrovirus. But evolution is built upon blind chance and cannot know ahead of time what kind of challenges will face the organism. This is like stumbling upon a tribe of isolated forest dwellers, one of whom can speak perfect English with you. It is more likely that piRNA already existed within the host genome as a design element to keep the levels of the KoRV in check. Citation required.
Why creation is a better explanation
It is possible to reinterpret retroviruses according to creation theory. Accordingly, retroviruses could have originated from within the host genome instead of invading it from outside. This had to have been the case in any scenario, since viruses are dependent upon host cells. This means that the cell’s genome had to predate viruses. Viruses are incapable of surviving without a host cell. That is, the ERVs are more likely rogue products of the genomes of their hosts. And the parts of genomes that look like ERVs are then seen as designed to do what they do (and well).
The jury is out whether the ancestors of viruses came before or after non-viral life. It could be that viruses came first, but lost the ability to ‘live’ and replicate on their own, like many parasitic organisms, or after, deriving from the cells of living organisms. Either way, it is irrelevant. ERVs derive from retroviruses, whatever their origin, and are heritable, proving common ancestry among those organisms that share them in the same DNA loci.
Research (by “evolutionists’. Creationists don’t do research. They are too afraid of proving themselves mistaken.) will increasingly reveal the functions of these misnamed ‘retrovirus elements’. Dr Ian Macreadie, at the time researching the retrovirus HIV, suggested this way back in 1999.
Since viruses take up such a large portion of the genome, they must have some sort of function. Viruses are capable of transporting genes besides their own between bacteria, for example.
According to the variation-inducing genetic element, or ‘VIGE’ hypothesis, certain genes in host genomes do not originate from retroviruses from outside. Rather these genes are infuenced by transposable genetic elements, which can alter the regulation of genes. When these transposable elements leave copies of themselves behind, they ensure that the new variation that they brought about can be inherited.
Here are the questions that must be answered for those who think that ERVs are not derived from retroviruses, but designed.
a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that produced the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV?
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people certain HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages?
k) Why use reverse transcriptase to copy RNA to DNA when, as we know, the reverse transcription process is error-prone, with no error detection and correction?
l) Why use integrase to insert potentially erroneous DNA in virtually random locations, often disrupting the genetics already there?
m) Why did it take humans, rather than a magic being, to create CRISPR/Cas9 technology for precise gene editing?
The transposable elements which cause the variation within the host genome are the gag and pol genes. The gene that they regulate is the env protein. The syncytin gene is attached to the env gene of the so-called ERV-W element which is expressed in a part of the placenta called the syncytiotrophoblast. Yet another regulatory transposable element called the trophoblast speci c enhancer (TSE) is responsible for expressing the syncytin gene only in the placenta and nowhere else. Syncytin is essential for successful pregnancy, so how did mammals reproduce before the putative ERV- W infected the mammal line and then fortuitously developed this function? It is all rather fanciful wishful thinking on behalf of evolutionists. They reproduced perfectly well without placentae, just as many other species still do.
Conclusion
Evolutionists claim Scientists have found that a large portion of the human genome is littered with remains of viral infections, with remains of virus DNA littered here and there. This has never been observed experimentally, so researchers must look elsewhere to see if this process really does take place in nature.
Here is an experiment that proves that ERVs derive from retroviruses. https://genome.cshlp.org/content/early/2006/10/31/gr.5565706.full.pdf+html
Evolutionists claim Scientists observe that retroviruses such as the koalavirus are invading the genome of their host species. They say that this way these viruses can help the evolution of the host genome by inserting novel DNA into it. This idea is rather implausible. It goes against the logic of natural selection, because the koalas become sick due to viral infection. Therefore, those koalas infected with the virus would be eliminated, together with any copies of the virus with them.
Again, nobody is claiming that KoRV is good for koalas, quite the opposite. But by Cserhati’s “logic” all pathogens should be extinct, having wiped out all their potential hosts. No. For natural selection to work, the virus would have to be fatal to all individuals, and to kill them before they reproduced. It would be nice to live in a world without pathogens, but it is not the world we live in.
But there is a second hurdle at the cellular level the koalavirus must jump before it can fully get integrated into the genome of its host. This is a molecular selection system, which eliminates genes which the cell does not recognize as its own. This involves special RNA molecules which bind to the virus genes, thereby removing them from cellular traffic and making it impossible for them to become a permanent part of the host genome.
Citation required (or you are just making stuff up again).
Certain mobile retrovirus particles originally could have moved from site to site within the genome, thereby changing the way genes are regulated within the host genome. It makes much more sense if retroviruses were originally designed as part of the host genome and escaped from the cell after the accumulation of a mutations.
Did anyone proofread that for you?
If viral DNA is inserted at random into the genome, it is much more likely to disrupt existing genes. A blindfolded painter will most likely mess up the painting he is working on by just applying random brushstrokes to it.
See my reference to Huxley and natural selection above.
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