More on the Design Hypothesis

Barry: If anyone thinks that ERVs are designed for a purpose or for several purposes, they must have answers to the following.

Riaan: I never claimed all ERV's are designed, stating as a fact, that the insistence that these are in fact from viruses, is inserted, not demonstrated.

Barry: Then why are you trying to answer these questions? The reasons why we know that they are retroviral integrations may be found here, @ https://barryhisblog.blogspot.com/p/why-do-virologists-and-geneticists.html 

Barry: a) What is reverse transcriptase designed to do? Why was it designed? To what purpose?

Riaan: it's function. RNA being able to transcript into DNA doesn't mean all claimed ERV's arose this way. That's your assumption.

Barry: Retroviruses have reverse transcriptase to copy their RNA genomes into DNA to integrate with a host cell's DNA, in order to induce the host cell to generate new retroviruses. There is no other explanation for it. 

Barry: b) What is integrase designed to do? Why was it designed? To what purpose?

Riaan: again, the ability for RNA to affect DNA does not mean all supposed ERV's are in fact vital in origin.

Barry: Integrase is required to perform the integration of the retroviral provirus with the host's DNA. Again, there is no other explanation for it. 

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

Riaan: Don't know, why did ERV's evolve. The question does not mean all supposed ERV's are in fact viral.

Barry: That wasn't the question. Viruses exhibit a viral codon bias. So do endogenous retroviruses. The explanation is simple and obvious.

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

Riaan: because that's how DNA functions, you won't have life without it. Do you think this is somehow related to ERV's specifically?

Barry: LTRs are promoters, found in exogenous retroviruses, in proviruses in somatic cells, and in ERVs. RNA polymerase does not normally transcribe promoters, but the replication of LTRs is essential to the retroviral replication cycle. LTRs are part of the 'hack' that preserves them through the replication cycle, and only make sense as part of the retoviral 'hack'.

Barry: e) What were the HERVs that produced the consensus sequence that generated Phoenix designed for?

Riaan: no clue what three F@#$ you're in about.

Barry: Then you need to find out, if you want to discuss the subject. An explanation can be found in my FAQ. See https://barryhisblog.blogspot.com/p/whats-all-this-about-phoenix-virus.html

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

f) you're essentially asking WHY, viruses where designed. Why did they evolve? Meaningless question unrelated to the argument whatsoever.

Barry: That's not what I'm asking. And common ERVs prove common ancestry however they originated. 

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

Riaan: again, were discovering the functions of so called ERV's ever more. Are you denying the clear functionality we've discovered so far? What we have not seen is anyone prove that all these supposed ERV's are in fact from viruses. You're seemingly mistaking an inferences for a fact. Tsk tsk tsk. You should know better shouldn't you?

Barry: Yet another non-answer. The question was about common disabling mutations, not about function, which are discussed in depth in the FAQ. See https://barryhisblog.blogspot.com/p/the-not-junk-efence.html

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

Riaan: more nonsensical questions with zero relevance to the actual discussion, trying to overwhelm with supply questions I see...

Barry: No answer yet again. If ERVs were part of an original genome design, we would expect to see them in every healthy individual. And we certainly should not see LTR-LTR discontinuities of varying degrees in different ERVs. See https://barryhisblog.blogspot.com/p/long-terminal-repeats-ltrs.html

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

Riaan: because not animals embryology USA the same, rather obvious, and again, unrelated.

Barry: A syncytial layer does exactly the same job, whether the syncytin derives from one retroviral env gene or another. Same design, same designer? Not here. They aeke no sense as designed features.

Barry: j) Why would an intelligent designer need to use a retroviral vector for altering intelligently designed genomes?

j) predicated on the inference that all these are in fact retroviral. Smh. Citations of FACT requires PROOF. GOT ANY?

Already given. See above.

Barry: 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?

k) again a meaningless question with no particular relevance to the subject. I can ask the same thing of you, with similar irrelevance.

Well, it is rather a puzzle, a supposedly intelligent designer using such a hit-and-miss shotgun approach to modifying genomes, wouldn't you agree?

Barry: l) Why use integrase to insert potentially erroneous DNA in virtually random locations, often disrupting the genetics already there?

l) why create disease... Smh. Again irrelevance to the actual discussion.

So you have no answer.

Barry: m) Why did it take humans, rather than a magic being, to create CRISPR/Cas9 technology for precise gene editing?

m) there we go, ask meaningless questions that reveal your purpose perfectly... Why insist random processes can produce what the humans smart enough to create CRISPR cannot do? Smh.

No idea?