https://barryhisblog.blogspot.com/p/this-booklet-is-from-certain-donny-b.html
This booklet is from a certain "Donny B." and "Matt Naylor", a pair of creationists who collectively and ironically style themselves as "Standing for Truth".
Endogenous retroviruses (ERVs) are stretches of DNA embedded in our genomes, and are some of the clearest and most solid scientific evidence for common ancestry, for example, and notably, between humans and chimpanzees.
There are things that come up in this review that are inevitably somewhat technical. There isn't scope here to go into what all this means in detail here, but there is plenty of good material in print and online.
The book is a slim volume with much that has been cut and pasted from other sources. It is also somewhat repetitive and contains rambles which are not relevant to the topic. It could probably have been a third of the size that it is, or even less.
It begins with the common creationist go-to argument that certain elements of certain ERVs perform useful and often vital functions for their host organisms. This, they claim, in Paleyan fashion, "proves" that ERVs have been designed into host's genomes. At the same time they often push, inconsistently, the fake narrative that "evolutionists" (non creationists) depend on an argument that ERVs are useless junk. It is "evolutionists", and not creationists who have researched these functions and have published their results. To claim that they have not is inexcusable.
They talk of "reason and purpose" in ERV elements, but not the reason and purpose agreed on by the entire scientific community - that they descend from retroviruses whose "reason and purpose" is to get host organisms to create more retroviruses.
Pretty well all the evidence for the fact that ERVs descend from retroviruses is absent in this booklet. This is the norm for creationist "literature" on the subject of ERVs.
The scientific evidence is
1) retroviruses in the environment (exogenous retroviruses) and ERVs exhibit exactly the same genetic elements, all oriented to the well-understood process of retroviral replication (albeit that ERVs may be partial or damaged - the reason why they have survived in our genomes and not been flushed out by negative selection.
2) ERVs exhibit a retroviral codon bias, just as exogenous retroviruses do.
3) certain elements in both exogenous and endogenous retroviruses sport "LTRs" (long terminal repeats, vital to, and only making sense in, the context of retroviral replication.
4) A fully functional exogenous retrovirus has been resurrected by fixing mutations to ERVs. This is what is popularly called the "Phoenix" virus experiment.
5) A retrovirus has been caught in the act of invading the heritable genomes of koalas.
In the cases or 4) and 5) above, the relevant papers are cited, but there is no discussion of them. I suspect that the writers haven't understood the scientific literature, or haven't even read it, and hope that adding scientific citations will convince the gullible that the writers are being "sciencey", trusting that their readers will not go to the sources, or not understand them if they did.
But out, again, come the usual bleats about function. ERV elements are involved in
1) embryology
2) immunity
3) generating genetic diversity
With any of these functions, the scientific argument is that
1) only parts of some ERVs serve the host. What is all the rest for?
2) it should be understandable that, given that retroviral replication is error-prone, the process can be expected to generate variants of genes that may just happen to be useful, and will therefore benefit from positive selection.
But specifically, embryology: There is a gene found in both exogenous and endogenous retroviruses, called the 'env' or envelope gene. This allows a retrovirus to merge with a host cell. This is the first part of the infection process. An interesting fact is that HIV's env gene is used to merge further T-cells with the cell it first invaded, creating a "syncytium", a super cell structure that includes the nuclei of all the cells it has absorbed. This is exactly the same thing as we see in the syncytial layer in the placenta. An enzyme, syncytin, is responsible for its formation. Where do we find it? In the exact location in an ERV, where you would find an env gene in an exogenous retrovirus! And that is not all. Different syncytins, in different ERVs, in different chromosomes have been found in different placental lineages. All have been found in the exact same spot within each ERV where an env gene should be! Nature has performed this trick more than once.
Immunity: The writers wonder about what is called superinfection resistance in ERVs, protecting the cell from - well - superinfection. Surely this is designed in? Well, no. There is a perfectly good evolutionary rationale for this. Basically, it's the predator (the virus) protecting its capture. And it is there whether the provirus (the DNA version of the virus), is in a somatic cell or a gamete. In other words, its "function" is not designed into host genomes. If it is "designed into" anything, it is "designed into" the exogenous retrovirus.
We come, lastly, to the silliest, most unworkable design idea of them all, "ERVs are for generating genetic diversity": This can be dismissed in very few words. The idea is that ERVs (or some ERVs) were designed into our genomes in order to create exogenous retroviruses that would reinfect our cells in new locations to create more diversity for evolution to work on. "For evolution to work on"? Aren't you guys supposed to be creationists? The process of endogenization is error prone. There is no error checking, let alone correction. The locus of the integration (the place where the retroviral material is inserted in the host DNA), is basically uncontrollable. It's like dropping a bull in a china shop. No intelligent designer (or human therapist) would use such uncontrollable and dangerous tools. And which are supposed to be the original ERVs, and which are supposed to be the result of their re-endogenisations? How do you explain their appearance of orthology in different species? The idea doesn't make your problem go away.
Endogenous retroviruses (ERVs) are stretches of DNA embedded in our genomes, and are some of the clearest and most solid scientific evidence for common ancestry, for example, and notably, between humans and chimpanzees.
There are things that come up in this review that are inevitably somewhat technical. There isn't scope here to go into what all this means in detail here, but there is plenty of good material in print and online.
The book is a slim volume with much that has been cut and pasted from other sources. It is also somewhat repetitive and contains rambles which are not relevant to the topic. It could probably have been a third of the size that it is, or even less.
It begins with the common creationist go-to argument that certain elements of certain ERVs perform useful and often vital functions for their host organisms. This, they claim, in Paleyan fashion, "proves" that ERVs have been designed into host's genomes. At the same time they often push, inconsistently, the fake narrative that "evolutionists" (non creationists) depend on an argument that ERVs are useless junk. It is "evolutionists", and not creationists who have researched these functions and have published their results. To claim that they have not is inexcusable.
They talk of "reason and purpose" in ERV elements, but not the reason and purpose agreed on by the entire scientific community - that they descend from retroviruses whose "reason and purpose" is to get host organisms to create more retroviruses.
Pretty well all the evidence for the fact that ERVs descend from retroviruses is absent in this booklet. This is the norm for creationist "literature" on the subject of ERVs.
The scientific evidence is
1) retroviruses in the environment (exogenous retroviruses) and ERVs exhibit exactly the same genetic elements, all oriented to the well-understood process of retroviral replication (albeit that ERVs may be partial or damaged - the reason why they have survived in our genomes and not been flushed out by negative selection.
2) ERVs exhibit a retroviral codon bias, just as exogenous retroviruses do.
3) certain elements in both exogenous and endogenous retroviruses sport "LTRs" (long terminal repeats, vital to, and only making sense in, the context of retroviral replication.
4) A fully functional exogenous retrovirus has been resurrected by fixing mutations to ERVs. This is what is popularly called the "Phoenix" virus experiment.
5) A retrovirus has been caught in the act of invading the heritable genomes of koalas.
In the cases or 4) and 5) above, the relevant papers are cited, but there is no discussion of them. I suspect that the writers haven't understood the scientific literature, or haven't even read it, and hope that adding scientific citations will convince the gullible that the writers are being "sciencey", trusting that their readers will not go to the sources, or not understand them if they did.
But out, again, come the usual bleats about function. ERV elements are involved in
1) embryology
2) immunity
3) generating genetic diversity
With any of these functions, the scientific argument is that
1) only parts of some ERVs serve the host. What is all the rest for?
2) it should be understandable that, given that retroviral replication is error-prone, the process can be expected to generate variants of genes that may just happen to be useful, and will therefore benefit from positive selection.
But specifically, embryology: There is a gene found in both exogenous and endogenous retroviruses, called the 'env' or envelope gene. This allows a retrovirus to merge with a host cell. This is the first part of the infection process. An interesting fact is that HIV's env gene is used to merge further T-cells with the cell it first invaded, creating a "syncytium", a super cell structure that includes the nuclei of all the cells it has absorbed. This is exactly the same thing as we see in the syncytial layer in the placenta. An enzyme, syncytin, is responsible for its formation. Where do we find it? In the exact location in an ERV, where you would find an env gene in an exogenous retrovirus! And that is not all. Different syncytins, in different ERVs, in different chromosomes have been found in different placental lineages. All have been found in the exact same spot within each ERV where an env gene should be! Nature has performed this trick more than once.
Immunity: The writers wonder about what is called superinfection resistance in ERVs, protecting the cell from - well - superinfection. Surely this is designed in? Well, no. There is a perfectly good evolutionary rationale for this. Basically, it's the predator (the virus) protecting its capture. And it is there whether the provirus (the DNA version of the virus), is in a somatic cell or a gamete. In other words, its "function" is not designed into host genomes. If it is "designed into" anything, it is "designed into" the exogenous retrovirus.
We come, lastly, to the silliest, most unworkable design idea of them all, "ERVs are for generating genetic diversity": This can be dismissed in very few words. The idea is that ERVs (or some ERVs) were designed into our genomes in order to create exogenous retroviruses that would reinfect our cells in new locations to create more diversity for evolution to work on. "For evolution to work on"? Aren't you guys supposed to be creationists? The process of endogenization is error prone. There is no error checking, let alone correction. The locus of the integration (the place where the retroviral material is inserted in the host DNA), is basically uncontrollable. It's like dropping a bull in a china shop. No intelligent designer (or human therapist) would use such uncontrollable and dangerous tools. And which are supposed to be the original ERVs, and which are supposed to be the result of their re-endogenisations? How do you explain their appearance of orthology in different species? The idea doesn't make your problem go away.
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