If ERVs are designed, what are the design purposes of these features? Another attempt.

Well as far as ERVs being designed I really can't say why they were designed the way they are. I don't have an extensive knowledge of ERVs. Though I do understand viruses in general.
I won't make the arrangement that they are indevidualy designed for any specific purpose. However i really don't see them as any evidence for ancestry.
In your argument you claim that common ERVs between Chimps and Humans indicate that they have a common ancestor.

In order to make this conclusion don't you have to assume that the ERVs and Viruses had to originate from outside the cell or genome. But we know that they can't replicate with out being inside a cell. Thus it seems to me that it would be more likely that ERVs and all viruses originate from genomes within cellular organisms.

What if the common ERVs in Chimps and Humans are simply parts of their original designed genomes and since most of the human and chimp genomes were originally similar than they would also share the same ERVs in the same places.

You are asking questions that don't necessarily need to be answered and you answered them your self. You are essentially suggesting that design throeists need to come up with some other design function than that given in virology.
What if they were designed to do exactly what Virology has determined they do.

Thus to answer questions a) and b) their design is the same as your answers.

>Here are my questions, together with my answers.
>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. It's 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.

>It seems that you aretrying to answer the questions by going for the "VIGE explanation". This is an acronym I have only ever seen in creationist literature, and never in any scientific literature. It stands for "Variation Inducing Genetic Elements". The idea is that our genomes were designed with retroviral proviruses designed in. The purpose of them is to create exogenous retroviruses, which will then invade organisms' genomes and integrate new variations. There are a number of problems with the "VIGE hypothesis" which means that it cannot make any sense. The main problem for creationists is that it cannot explain common loci in what must be re-integrations, thus you are still left with the problem of explaining them.

>See "Could you have this backwards? Maybe retroviruses come from designed-in variation inducing genetic elements (VIGEs)?"

For c) obviously they were designed with viral codon biases so that they could function as a virus. Without the virus codon biases they woul likely just be considered a part of the genome. Also they might not be able to move to other parts of the genome.

>The question was, c) Why were ERVs designed with a viral codon bias?

>The explanation is that they originate from viral genomes.

>A different codon bias would make no difference to the functioning of the viruses. 

For the answer to d) and e) would again be the same as your answers.

>Which were

>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.

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

>They were "designed", originally, 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!

> so you are relying on "VIGE" agzin. As explained, it doesn't work as an explanation for commonly located ERVs

For f) you are taking a specific case and asking for its purpose while telling us that it has no purpose which means that you obviously don't know its purpose which leaves you in the same position. Also you are assuming that this specific ERV if designed. Must have been designed with a specific function.

>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). 

>The "purpose" of a retrovirus is merely to get itself replicated, like all viruses.

For g) If Chimps and humans were designed with common genomes and ERVs were a part of the common genomes than there is no need for any ancestral casual link. Your conclution to g) assumes your conclusion is correct inorder to make your conclusion.

>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 coincdentally is way beyond the bounds of credibility.

>You don't answer the question.

For h) it was likely designed that way to help create diversity. Also your final conclusion assumes your premise to be correct without rational or reason. You are arguing that we are only seeing a small fraction of the endogenization events. But this presumes that your final conclusion is correct that a lot of the species with such events went extinct. Unfortunately if they went extinct than we have no evidence to support the final conclusion thus the initial hypothesis/premise can't be falsified. If your initial premise isn't true then your final conclusion can't be either. This leaves such an argument unscientific according to your definition.

>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.

>"VIGE" yet again. 

For I) i don't know what syncytins are thus I really don't can't give any answer.

If ERVs or any virus originate from anywhere other than Cellular organismal genomes I would love to see the evidence showing how they where able to replicate or form without the cell.

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

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

>For an explanation of syncytia, see "ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?"