ERV FAQ: But how can you rule out design as an explanation?

https://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html

In science, we apply the principle of parsimony. This means that we go with the simplest hypothesis that accounts for the greatest amount of relevant data, and is contradicted by none of them. https://en.wikipedia.org/wiki/Occam%27s_razor

Regarding endogenous retroviruses (ERVs), endogenization fits the bill.
https://barryhisblog.blogspot.com/p/why-do-virologists-and-geneticists.html

'Design' does not. 

'Design' fails to explain why ERVs with the odd functional genes should be found in common locations in different species. Their location is not critical to their function.

https://barryhisblog.blogspot.com/p/arent-same-genes-in-same-places.html

'Design' fails to explain why long terminal repeats (LTRs) are so configured as to get themselves transcribed by RNA polymerase II. This is something that is essential to the retroviral replication cycle, but makes no sense as a 'designed' feature. https://barryhisblog.blogspot.com/p/long-terminal-repeats-ltrs.html

'Design' fails to explain such a scatter gun approach as using integrase to insert retroviral genes into host cells' DNA with no regard as to whether or not they will cause damage. 
https://barryhisblog.blogspot.com/p/integrase.html https://barryhisblog.blogspot.com/p/we-need-to-talk-about-integrase-with.html

A common tactic of creationists, writing about ERVs, (see this page, https://barryhisblog.blogspot.com/p/hasnt-evolutionists-story-about-ervs.html) is to suggest that ERVs were designed into the genomes of different "kinds" of organisms to provide a means of distributing useful genes by exogenization and re-endogenization. So which were the "original, designed-in" ERVs, and which were the result of exogenization and re-endogenization? How does "design" explain that the latter types are still in orthologous locations in different species? As we know, integrase is incapable of targetting specific DNA loci.

'Design' also fails to explain all the non-functional LTRs and ERVs. 

Endogenization in common ancestors explains all these things.

If you say, "Ah, well, it could be design, but we just don't know the reasons", then you have made your hypothesis unfalsifiable, and therefore of no interest to science. Under such a hypothesis, the actual facts become irrelevant. 

The purpose of science is to explain the actual facts - why they are as they are, and not otherwise.

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

a) What is reverse transcriptase designed to do? Why was it designed? To what purpose?
https://barryhisblog.blogspot.com/p/why-do-virologists-and-geneticists.html

b) What is integrase designed to do? Why was it designed? To what purpose?
https://barryhisblog.blogspot.com/p/integrase.html https://barryhisblog.blogspot.com/p/we-need-to-talk-about-integrase-with.html

c) Why were ERVs designed with a viral codon bias?
https://goldbio.com/articles/article/what-is-codon-bias#:~:text=Codon%20bias%20is%20a%20bias,cells%20or%20altering%20codon%20sequences.

d) What is the design purpose of re-transcribable promoters?
https://web.stanford.edu/group/nolan/_OldWebsite/tutorials/retcl_3_ltrs.html

e) What were the HERVs that produced the consensus sequence that generated
Phoenix was designed for?
https://pmc.ncbi.nlm.nih.gov/articles/PMC1665638/

f) What is the design purpose of both exogenous and endogenous KoRV? 
https://www.quantamagazine.org/koala-retrovirus-spreads-to-the-genome-20150304/

g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
https://toddcwood.blogspot.com/2009/10/microbes-continue-retroviruses.html

h) What is the design purpose of giving some people certain HERVs and not others?
https://www.pnas.org/doi/10.1073/pnas.1602336113 

i) What is the design purpose of creating different syncytia in different placental lineages?
https://barryhisblog.blogspot.com/p/ervs-are-essential-in-reproduction.html

j) Why would an intelligent designer need to use a retroviral vector for altering intelligently designed genomes?
https://barryhisblog.blogspot.com/p/could-you-have-this-backwards.html

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?

https://www.sciencedirect.com/science/article/pii/S0022283624004376#:~:text=1%2C%202%20RTs%20are%20multifunctional,%E2%80%B2%20exonuclease%20(proofreading)%20activity.

l) Why use integrase to insert potentially erroneous DNA in virtually random locations, often disrupting the genetics already there?
https://barryhisblog.blogspot.com/p/relationship-between-integration-sites.html

m) Why did it take humans, rather than a magic being, to  create CRISPR/Cas9 technology for precise gene editing?
https://www.yourgenome.org/theme/what-is-crispr-cas9/

See also - The "Not Junk" Anti-ERV Defence
and - More ancient viruses lurk in our DNA than we thought.

Someone attempted to answer these questions. I reply here. https://barryhisblog.blogspot.com/p/what-id-reverse-transcriptase-designed.html

And now "SFT" (the Beavis of the creationist Beavis and Butthed duo) has piped up with responses to these questions. I answer him here. https://barryhisblog.blogspot.com/p/standing-for-truth-attempts-to-reply-to.html

They had another go, which I examine here.

Yet another attempt is examined here. https://barryhisblog.blogspot.com/p/the-erv-design-hypothesis-more-answers.html

You see, it's no use just waving your arms in the air and saying, "Design". Endogenization explains all these features. Here is a page giving the explanations. How does 'design' explain them?

Endogenisation as an explanation.

https://barryhisblog.blogspot.com/p/endogenisation-as-explanation.html

The page, "But how can you rule out design as an explanation?" Asks a number of questions that a design hypothesis would naturally raise about ERVs.

The response from cdesign proponentsists has been almost completely silent. The few attempts made to answer the questions have been incoherent.

I thought it only fair to answer the same questions myself from the point of view of virology.

a) What is reverse transcriptase designed to do?

Reverse transcriptase, a retroviral enzyme, takes a viral RNA genome and uses the target host cell resources to make a DNA copy of it. The DNA copy is called the "provirus".

b) What is integrase designed to do?

Integrase is another retroviral enzyme. Its function is to snip the host DNA at some point, attach the DNA provirus to one of the resulting strands, and then join up the other strand at the other end of the provirus. Thus the provirus becomes integrated into the host cell's DNA.

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

Because they originate from viral genomes.

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

When a provirus is integrated, it includes all the genes required for the replication cycle to continue when it gets transcribed back into RNA. But it can't get the host cell to transcribe its genes back into RNA without transcription promoters, so these are included in the original viral genome. The trouble is, transcription does not normally work on promoters. The viral "design" includes a hack to make promoter transcription happen. This makes no sense in DNA that is not oriented to a retroviral replication cycle ('DNA + reverse transcriptase -> DNA + transcriptase -> RNA and so on, and so on.) These special promoters are called LTRs - long terminal repeats, and appear repetitively in large numbers at either end of a provirus or an ERV.

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

They were "designed", (or at least had the original features,) to get the host to produce new virions, but they became unable to do this because of mutations. The "Phoenix" experiment fixed these disabling mutations, and voilà, a fully functional retrovirus was resurrected! See https://barryhisblog.blogspot.com/p/whats-all-this-about-phoenix-virus.html

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

None. The exogenous retrovirus KoRv (Koala RetroVirus), its provirus versions found in somatic and germ-line cells has the same genome (in RNA form in the exogenous version, and in DNA form in the proviral and endogenous version). 

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

None. These mutations must have occurred in common ancestors. The idea that they happened coincidentally is way beyond the bounds of credibility.

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

None. When a retrovirus becomes endogenized at a particular locus, it happens in a single individual (in a single gamete!) Genetic drift, chance and natural selection determine how far it spreads through any offspring. The vast numbers of ERVs that are fixed (ubiquitous) in species must represent a small fraction of the number of endogenization events that have occurred, and many must have gone extinct.

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

None. The formation of syncytia is a native trick of some retroviruses (HIV is an example). Different retroviruses endogenized in different ancestral lineages and became exapted. 

https://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html