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.