The ERV Design Hypothesis. More Answers Offered.

Anne Gauger of the "Discovery Institute", a cdesign proponentsist pictured using green screen technology to push the lie that she works at a scientific laboratory.

"ERV" is an acronym for Endogenous RetroVirus. ERVs offer some of the best evidence for common ancestry among different "kinds" of animals, notably among humans and the other great apes. Go to the ERV FAQ to learn more. 

In my page,  But how can you rule out design as an explanation (of ERVs)? I raise a number of questions that a creationist/intelligent design hypothesis to account for them raises. Here, I look at a set of answers that a certain creationist proffered. I give him credit for his efforts. Other offerings are also linked to at the link just given.

The questions are lettered rather than numbered for reasons I forget. For a change, and for legibility, I have rendered our creationist's answers in red, and indented. Links in my questions link to additional information and explanation. To repeat them here in full would render the page far too "TLDR", but the devil, and the truth, is in the details. 

Let us begin.

Question a) What is reverse transcriptase designed to do? Why was it designed? To what purpose?
b) What is integrase designed to do? Why was it designed. To what purpose?

For questions a) and b) , I would venture that they are necessary to fix the ERV genes to the different loci as they moved about the genome, causing new variations / mutations, whilst they also aided the exogenised ERVs to attack other host organisms.

I can't see why a designer of our genomes would be forced to resort to such measures. Why not simply design in the features it wanted, like it is supposed to have done with the rest of our genomes? This is not parsimonious. But crucially, we know that integrase cannot target specific DNA loci. It is like playing Russian roulette with our genomes, which is why it is not used in gene therapy. It can disrupt important genes and also trigger cancers.

Question c) Why were ERVs designed with a viral codon bias?

For c), I would say the 'viral codon bias' was a post hoc discovery, post-Fall of created ERVs that were exogenised.

Pre or post hoc, it exists. There is no evidence for a "Fall", and plenty of evidence that ERVs exhibit a viral codon bias. The obvious explanation of a viral codon bias is that ERVs derive from viral genes.

d) What is the design purpose of re-transcribable promoters?

d) Transcribable promoters are essential to switching the 'ERV' on for their created purpose.

Retroviral promoters promote retroviral gene expression, essential for the retroviral replication process. 

e) What were the HERVs (human endogenous retroviruses) that produced the consensus sequence that generated Phoenix designed for?

HERV-K [A particular set of similar HERVs] probably had some benign use pre-Fall before it became malignant in purpose.

Again, there is no evidence for this "Fall". The HERV-Ks are not malignant, but inactive. Re-enacting them by fixing their disabling mutations renders them virulent (malignant). 

f) What is the design purpose of both exogenous and endogenous KoRV? 

Same reason as above, for KoRV

KoRV is clearly not part of any original koala genome. There are koalas without any endogenous traces of KoRV, and in those where it is endogenized, different koalas have endogenous KoRV ERVs in different regions of their DNA. This is all indicative of exogenous KoRV viruses endogenising in the koala population as we speak.

g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?

Probably the genomic purpose of those created ERVs in both those species was not necessary.

This answer rather goes against the idea that ERVs were designed for a purpose. 

h) What is the design purpose of giving some people certain HERVs and not others? 

The common HERVs in all humans were likely degraded in a non-uniform fashion. Genetic Entropy.

Sorry. This does not answer the question. We are not talking about degrees of degradation in designed in ERVs, but the fact that some people carry certain ERVs, and others do not. The obvious explanation is that certain retroviruses have endogenised, but have not gone to fixation in the human population. 

i) What is the design purpose of creating different syncytia in different placental lineages?

 Variation / Creativity of God on display.

The usual excuse for ERVs being found in common locations is that they were designed by some designer for a common purpose, and their locations are critical. Here, we have syncytia, not just in different loci, but in entirely different chromosomes, and with distinct contents. It is clear that these must have derived from different endogenizations by different retroviruses in different lineages. The fact that groups of creatures share the same syncytia in a lineage that other lines of evidence also indicate relatedness, and do not share the same syncytia with more distantly related lineages, is yet more evidence that the evolutionary view of ERVs (and evolution itself) is true.   

BTW, I was once in a FaceBook message exchange with Anne Gauger, on this subject. She asked me to cite the relevant scientific literature, which I did. (https://www.evolutionarymodel.com/ervs.htm#References). Her response? She immediately blocked me!