Essay:Endogenous Retroviruses

This page details how the endogenous signatures of retroviruses (ERVs) put common descent beyond any reasonable doubt.
It is presented in the form of an FAQ, answering the common objections of evolution-deniers.

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Adapted from Wikipedia:

"By the year AD 802,701, humanity has evolved into two separate species: the Eloi and the Morlocks. The Eloi live a life of ease on the surface, while the Morlocks live underground, tending machinery and providing for the Eloi. Having nothing they need to do, the Eloi have slowly become like cattle, smaller than modern humans with sub-human intelligence. All they do is feed, play, and mate. When one of them, Weena, falls into a river, none of the other Eloi help her. She is rescued instead by the Time Traveler. Every so often the Morlocks capture individual Eloi for food, and because this typically happens on moonless nights, the Eloi are terrified of darkness."

How would we prove that the Eloi and the Morlocks had indeed both descended from modern humans? Well, we have signatures in our DNA that were written by retroviruses.

They put their DNA into the DNA of our cells to "fool" them into making new retroviruses.

Sometimes, a retrovirus puts its DNA into the DNA of an egg or sperm cell. When this happens, it becomes heritable - you can inherit it from your parents and pass it down to your offspring. These heritable bits of viral DNA are called ERVs - Endogenous RetroViruses. Fortunately, they no longer fully perform their original functions, otherwise, humans would be extinct.

The signature of any endogenous retrovirus is that it can be found in exactly the same place in the DNA of every single one of your nuclear cells (every cell with a nucleus - which is most of them). The viral DNA ends up in the same place because it, along with all the rest of your DNA, is copied from the DNA of the original single cell you started out as. In contrast, the viral DNA that you have acquired from viruses in the environment is not present in all of your nuclear cells, and in those where it is present, the viral DNA ends up in different points in your DNA, comparing one infected cell with another.

To recap:

Viral DNA in the same place in the DNA of every cell means that it is inherited. Viral DNA in different places in only some of your cells means that you have caught a virus from the environment.

Now, if we find that all the Eloi have the same viral DNA as us, in every cell, in exactly the same places as us, we know that they must have inherited it from us, and therefore we are their ancestors.

The same goes for the Morlocks. The same viral DNA in the same places in every cell means that the Morlocks also descend from us.

Note that we do not even need to look at our own DNA! If we find the same viral DNA in the same places in the DNA of every cell of every Eloi and Morlock, they have to have had common ancestors from which they inherited it (us!).

Bear this in mind when the ERV FAQ mentions, not Eloi and Morlocks, but humans and chimpanzees!

What are "ERVs", and what is the "case for common descent" that they provide?

1. Retroviruses replicate by invading the cells of host organisms, converting their RNA genomes into DNA, and inserting (integrating, in the jargon) the DNA into the DNA of the host cell. The integrated DNA is called a "provirus". The host cell then "reads" the provirus, converting it back into RNA, resulting in the production of more viruses.

2. Retroviruses tend to target certain types of cells. Their "environment" proteins tend to be specialized to attach to the surfaces of these cells.

3. The integration into the host's DNA is made by a retroviral enzyme called integrase. While certain retroviruses can show a general tendency to insert their DNA in certain types of regions in a host cell's DNA, they do not target specific points (loci). This means that in an infected individual, not all cells will be infected, and in those that are, the retroviral integration will be in a different place or places in the DNA of each cell.

4. We find, in the genomes of creatures such as ourselves and chimpanzees, inherited structures that cannot be anything but the remnants of retroviral insertions. Some are more complete than others, but many have the full set of genes that would be necessary for a complete retrovirus, were they not faulty. We call these structures endogenous retroviruses (ERVs). Unlike the case where each cell is individually infected, they appear in the exact same spots in the DNA of every single nuclear cell (cells with nuclei containing DNA).

5. Although certain components of some ERVs perform functions in the host, some even being essential in some species, no complete ERVs are functional. Design, as an explanation for ERVs, does not make any sense. A designer would have no need to include specifically retroviral genes in its designs, which now do nothing, or may even cause harm. There would also be no need to design in non-functional traces of the action of integrase, traces of which are present in ERVs.

6. The only explanation that makes any sense is that ERVs are the result of retroviral insertions into germ-line DNA - egg cells or sperm cells, followed by reproduction and consequent cell division. Cell division will duplicate the ERVs in the same positions in the DNA of every cell. Separate, parallel infection would not infect every cell, and the proviruses would end up in different locations, comparing one infected cell with another.

7. All human beings have many thousands of ERVs and ERV fragments in the DNA of every one of their cells. Most of them are in identical DNA locations going from cell to cell, and person to person. This means that we all share common ancestors - the ancestors that first acquired each of the germ-line retroviral integrations.

8. All human beings and chimpanzees have many thousands of ERVs and ERV fragments in the DNA of every one of their cells. Most of them are in precisely corresponding DNA locations going from cell to cell, and individual to individual. This means that we all share common ancestors - the ancestors that first acquired each of the germ-line retroviral infections.

Why do virologists and geneticists think that ERVs come from retroviruses? Isn't that just supposition on their part?

Every detail of every full ERV is replete with complex and subtle details attesting to its origin in retroviruses. ERVs have the same structure as retroviral integrations. This is some -10 kilobases of genes specific to the retroviral replication cycle. All retroviruses and complete ERVs include genes we call gag, pol and env. The function of these genes will be gone into in detail in the following notes. In addition, several other features common to retroviral integrations and ERVs only make sense in terms of the requirements of the retroviral replication cycle.

The items in quotes come from Abbie Smith's excellent blog, https://scienceblogs.com/erv

"The gag gene encodes for ‘Gag’ the giant protein, which gets chopped into several smaller proteins, Matrix, Capsid, and Nucleocapsid (and sometimes a few more tiny ones, depending on the retrovirus)."

"Matrix is the structural protein just inside the envelope (the membrane the virus stole from its host cell). It has ‘outside’ functions (targeting the virus assembly to the right kind of cell membrane, keeping the outside protein env, in order) and ‘inside’ functions (targeting the reverse transcribed DNA to the new host cell nucleus). Jack of all trades protein, like lots of retroviral proteins. They run a tight ship."

"Capsid forms the viral ‘core’. Normally when you think of a ‘virus’, you think of this shape, an icosahedron. Retroviral ‘cores’ really look more like a cylinder-cone-thingie, like the bottom pic here. That particular pic is also worth a second look– More protein cuts to Capsid need to take place after a baby virus buds off from its host cell to make an immature virus mature. Blocking this maturation step is what the next family of anti-HIV-1 retrovirals do. *thumbs up*"

"Nucleocapsid is a structural protein that wraps up the retroviral genome to make sure its packaged properly into the Capsid."

Pol codes for all the enzymes a retrovirus needs:"

"Protease– Chomps big proteins into all the little functional proteins, like we saw with Gag getting chomped into Matrix/Capsid/Nucleocapsid. The name ‘protease’ can be a little confusing because all organisms have ‘proteases‘, but only the protease that the retrovirus carries with it is the ‘right‘ protease to cleave in all the ‘right’ spots to get all the ‘right’ proteins in the end. Instead of giving retroviral proteases a special name, they just named it ‘Protease’. heh. Protease inhibitors are a great target for anti-retrovirals."

"Reverse Transcriptase– Another target for anti-retrovirals. Though the process of reverse transcription can be found in you and I (coooool), retroviruses need to carry an enzyme with them to convert viral RNA into DNA on demand. This process not only requires converting an RNA genome into a DNA genome, but also:"

"RNase H– The RT enzyme has (at least) two active sites. One performs the process of reverse transcription. Another active site has RNase activity (chops up RNA, specifically, RNA Hybridized with DNA haha!). RNase H chews up the old RNA template after a single strand of DNA has been made, so the single strand of DNA can be made into double stranded DNA, and subsequently inserted into the host cells genome. This might make more sense if you see this animation. *might* The process of reverse transcription is rather absurd."

"Integrase– Host cells don't come packed with the necessary biochemical machinery to move DNA out of the cytoplasm into the nucleus, to be inserted into the host DNA. So once again, retroviruses need to bring an enzyme capable of performing those activities. Integrase should be a perfect target for antiretrovirals… But we havent figured any out yet…"

Env. See http://scienceblogs.com/erv/2008/07/17/intro-to-ervs-envy-my-env/

LTRs. See this page. RNA polymerase's normal function is to convert nuclear DNA into messenger RNA that makes for proteins. It does not normally make RNA that 'codes" for promoters. Our bodies have no need for them. But retroviruses need their promoters to be converted back to RNA for when the replication cycle begins again. Long terminal repeats (LTRs) cause the RNA polymerase to produce them by a complicated "hack". The point is, that LTRs basic and original function is a part of the replication process of retroviruses. They cannot be part of any supposed original "design" of our genomes. That would not make any sense.

See http://barryhisblog.blogspot.fr/p/ervs-promote-transcription-of-host-dna.html and http://scienceblogs.com/erv/2009/07/16/intro-to-ervs-ltr-gator

Retroviruses exhibit the distinctive viral codon bias.

The Phoenix virus was resurrected from the multiple instances of an ERV which is to be found in each human cell. Each instance is a 'failed' retrovirus, but when a 'majority vote' for each base was taken, the resulting DNA produced, "viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny." See also The "Phoenix Virus": an explanation of an experiment.

A retrovirus has been caught in the act of becoming endogenized: See The koala retrovirus KoRV and The Koala's Tale.

Retroviruses leave a telltale trace of integration in the form of a repeated host sequence either side of the integrated provirus. This is also evident in ERVs. From Virology Blog: Retroviral Integration and the XMRV Provirus, "The image below shows some of the characteristic features of retroviral integration. A the top is the unintegrated linear DNA of avian sarcoma/leukosis virus produced by reverse transcription. Upon completion of integration, two base pairs (AA•TT) are lost from both termini, and a 6-bp target site in host DNA (pink) is duplicated on either side of the proviral DNA. This target site varies in length from 4 to 6 bp among different retroviruses. The proviral DNA (middle) ends with the conserved 5′-T G…C A-3′ sequence. The provirus serves as a template for the production of the viral RNA genome (bottom)."

Isn't this just circular reasoning, assuming evolution to 'prove' evolution?

No. No assumption of evolution is made when concluding that commonly located ERVs are due to common ancestry.

A conclusion drawn from evidence and reasoning is not an "assumption" or a "presupposition".

The conclusion is drawn from the following items of evidence -

1. ERVs have the same detailed structure as proviruses. This fact does not require us to assume evolution.
2. Retroviral integration does not target specific loci in DNA. This fact does not require us to assume evolution.
3. Inheritance places the same genetic material in the same locations in DNA. This fact does not require us to assume evolution.

How many ERVs are shared, in common locations, in the genomes of humans and chimps?

From table 11 of Initial sequencing and analysis of the human genome, ERVs found in humans (HERVs) include

• 112,000 ERV-class Is +
• 8,000 ERV(K)-class IIs +
• 83,000 ERV(L)-class IIIs
• = 203,000 ERVs.

From table 2 of Initial sequence of the chimpanzee genome and comparison with the human genome, 279 of the 203,000 ERVs are specific to chimps, and 82 are specific to humans.

The vast majority of the 203,000 ERVs are common to chimps and humans, and appear in precisely corresponding loci in our genomes. See Amount of shared ERVs.

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  Caption1

• Transposable element activity in human and chimpanzee lineages. jpeg

  Transposable element activity in human and_chimpanzee lineages

Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?

Creationists will clutch at studies that show "target site preferences" that retroviruses might exhibit, such as transcriptionally active regions of the genome in order to try and explain away commonly located ERVs in different species. But these do not explain the precisely corresponding loci that endogenous retroviruses exhibit in related species. This precision in corresponding ERVs is not a general statistical preference for certain types of regions, but is exact down to the resolution of single base-pairs. It is like studying road traffic accidents, and finding certain areas, "accident black-spots" in which accidents are more likely to occur. Reports of accidents occurring in the same general area, at different times, involving different people and vehicles, are obviously different accidents. But reports of accidents, from those involved, from witnesses, police and medics all agreeing on the exact, precise details of the accident, are clearly different reports of the same accident. Similarly, an identical retroviral integration in precisely the same locus in different organisms says that these are all copies of the same original integration.

Here's a summary of a study of integration sites.

Relationship between Integration Sites and Transcriptional Intensity in the Human Genome from DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences The human chromosomes are shown numbered. HIV integration sites are shown as blue “lollipops”; MLV integration sites are shown in lavender, and ASLV integration sites are shown in green. Transcriptional activity is shown by the red shading on each of the chromosomes (derived from quantification of nonnormalized EST libraries, see text). Centromeres, which are mostly unsequenced, are shown as grey rectangles.

It would be great if we could use retroviral-like vehicles to precisely target positions in DNA. Think of the possibilities that would open up. It would be a wonderful tool for gene therapy, including cancer treatment, treatment for genetically inherited diseases, anti-viral therapy, genetic engineering, and pure research. That, and the search for possible ways to tackle retroviral integration, is why it has been studied so carefully. Unfortunately, integrase, the enzyme that actually does the integration of a new DNA sequence into the DNA of the host organism, does not target specific loci. Recent techniques developed for precise gene editing do not use retroviral-native integrases.

Actual studies of integration sites include HIV integration site selection: Analysis by massively parallel pyrosequencing reveals association with epigenetic modifications and Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences and many others. While the title of the second paper sounds interesting from the creationist point of view, it doesn't help. What these sorts of studies do is to survey real retroviral integration sites, using the same types of cell from the same individuals (identical DNA) in order to find any statistical 'preference' for certain types of area (in an existing gene, not in a gene, near a promoter etc.) Typically, they find some overall patterns, but no repetition of integration sites within 500 samples of the same cell type with the same retrovirus. This is not the locus specificity required to account for 200,000 integrations in precisely corresponding loci. Only common inheritance can account for them.

ERVs do stuff. Doesn't that prove that they didn't originate from retroviruses, but were designed?

Lots of DNA does stuff, whether it is a part of an ERV or not. If you were to point to something and say, "that looks designed for a purpose", you would do better to point at the genes for vision, say, or digestion. ERVs make no sense from the design point of view. Only bits of some ERVs do anything, and what they do is not always helpful. Why are the other bits there, and why are all the other ERVs there, the ones that have no functional bits? Why do they all have all the hallmarks of retroviral integrations? (See "Why do virologists and geneticists think that ERVs come from retroviruses?"). When you look at ERV function in any of the other sections of this FAQ, ask yourself, "Does this make sense as a by-product of retroviral action, or as something designed to meet a specific purpose?"

It makes sense for evolution to co-opt useful endogenous retroviral DNA. Detrimental elements will be flushed out of the genome by negative selection. Neutral elements will drift, get chopped up and mutated. Useful elements will tend to increase in frequency in the population generation by generation. An ERV that has lost the ability to replicate complete viruses is in the same evolutionary "boat" as all the rest of the organism's genome. It can't replicate via transcription any more - the route used by functional retroviruses. It's "ticket" into the next generation is the same ticket as all the rest of the organism's DNA - to be useful, or if you can't be useful, be lucky, and get replicated along with all of the rest of the organism's DNA.

Function is often cited as a rationale for common loci between species. This is based on a misunderstanding of how genetics works. Genes and their promoters can exist almost anywhere on any chromosome, and they will work in the same way. There is no inherent functional reason for corresponding loci in two different species. See Aren't the same ERV genetics in the same places in different species because they have to do the same job?

See also, "ERVs promote the transcription of host DNA. Doesn't this prove they are designed?" and "ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?"

ERVs promote the transcription of host DNA. Doesn't this prove they are designed?

Integrated retroviruses have two identical regions, one at each end of the integration, called long terminal repeats (LTRs). These perform two functions, the first to promote the transcription of retroviral genes within the host cell and also to cause transcription back into RNA of all the non-protein coding parts of the provirus, without either of which functions, the retrovirus would not get replicated. This latter task is particularly tricky and complicated, and the LTR promoters must have specific features to fulfill it. A promoter that was designed to promote "native" DNA would not need these retroviral-specific features.

As mentioned above, promoters are essential for getting retroviral genes transcribed. Retroviruses don't "care" if an incidental by-product of dropping a promoter into the genome is to promote some "native" genetics as well. Drop a promoter into a genome, more or less at random, and there is a god chance that it will promote something or other. Natural selection will "decide" whether that promotion activity is bad news, or not.

Not all ERV LTRs promote transcription, not by a long way and among those that do, many of the the resulting transcripts either serve no identifiable purpose or are implicated in late-onset diseases.

The main thing that LTRs do, when they do anything, is to promote transcription. That does not mean that all the transcripts do anything useful. Some will. Some won't. Some are implicated in late-onset diseases. The structure of an LTR in a retrovirus is specific to a tricky problem retroviruses face in getting transcribed once again. That structure makes no sense as a designed promoter for native genes. It makes no sense to have useful, useless and dangerous transcripts lying about. It makes no sense to scatter the genome with ERVs, only some of which provide promoters that promote anything. It makes no sense to attach to those promoters sets of genes that pertain solely to the retroviral replication cycle - namely reverse transcriptase and integrase. If I wanted to argue that some aspect of the human genome was designed, I would not point to ERVs. They make no sense whatsoever as designed features.

ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?

See Abbie Smith's blog entry, "More syncytia sweetness". Primates, mice and sheep each use a different syncytin gene, from the env region of a different ERV, in a different chromosome, in order to build an essential syncytia in the placentas of their respective lineages. (A syncytium is a cell that contains many cellnuclei, as opposed to normal nuclear cells, which usually contain only one cell.) Why different syncytins from different ERVs? Different designs, different designers? Hardly. And why embed the syncytins in ERVS in the first place? What's all the other ERV baggage for?

It turns out that syncytia formation is a native trick of retroviruses. HIV will deal with attacking T-cells by absorbing them into the cells it has already infected. How? By attaching them to itself and joining with them, using the very same env proteins it used to enter the original cell! Clever trick. It avoids all the tedious business of invading every T-cell in order to neutralize them.

Note that the different syncytia belong to different lineages - further proof of evolution. We can even trace their evolution through their respective family trees. See also, Mammals Made by Viruses. Why on earth would a designer take such pains to mimic the the sort of thing we expect from evolution - for no sensible reason? Why did it not mix things up a bit? Why did it never choose to produce any evidence contrary to what we would expect of evolution? See also, Gauger's Gaffe!

Still think ERVs are not of retroviral origin? If so, you must have answers to these questions: If ERVs are not retroviral in origin, why do they have reverse transcriptase? What do they have integrase? Why do they have LTR promoters? Why did the Phoenix virus experiment work? Why do ERVs have host DNA repetition on either side of the integration site? Why do koalas have KoRV in both exogenous and endogenous form? Why do ERVs have the same codon bias as retroviruses? See also, The Koala's Tale.

It always amazes me when people say, look! These endogenous promoters or genes do something. It _proves_ they are designed! Bits and bobs of some ERVs. Never a whole working ERV (which would likely kill you). If we don't accept that eyes were designed, just because they are useful, why would we conclude that ERVs are designed, just because the odd component has been scavenged from them? When we look at the human/chimp syncytin gene, and consider it's origin, there are two possibilities.

1. A designer or designers inserted it in the genome of both species, in exactly corresponding locations in the DNA (unnecessarily), the syncytin gene being embedded in an elaborately detailed structure that precisely, and pointlessly mimics a retroviral insertion. (See "Why do virologists and geneticists think that ERVs come from retroviruses?") A designer or designers also inserted a different syncytin, in a different location, in a different chromosome, precisely and pointlessly mimicking a different retroviral insertion in mice. And a completely different one again in sheep. The supposed designer(s) didn't bother with Elephants. Or Manatees. Or heteromyid rodents. They were designed to get along without a placental syncytiotrophoblast layer, relying instead on a layer consisting of discrete nuclear cells (cells with a single nucleus each).

2. A common ancestor of chimps and humans, its species happily reproducing like elephants, acquired a retroviral infection in a germ-line cell. When it came to reproduce, one of the retroviral genes woke up and affected the development of certain placental cells, having the effect of merging them into a single multi-nucleus cell (a syncytium) just as the corresponding gene in HIV does with T-cells today. This aided reproduction, giving an advantage in the reproductive stakes, such that more and more individuals inherited the trick, and it eventually became a ubiquitous (fixed) feature in the species. At the same time it was spreading through the population, older genes for placental development that were no longer needed mutated into uselessness, rendering the new retroviral gene (but not the rest of its accompanying retroviral baggage) essential. The same thing happened, but with a different retrovirus, in mice. And again, independently, with a different retrovirus in sheep. It did not happen in pigs, or in horses. Which of the above two scenarios best explains the retroviral-like structure that is to be found at the site of the human/chimp syncytin gene?

See also, True facts about marsupials.

Aren't the same ERV genetics in the same places in different species because they have to do the same job?

No.

It is a common misconception that the genome is one vast integrated machine.

It's not how it works. A more accurate image would be one of a collection of recipes.

Every cell with chromosomes (every cell with a nucleus - (every nuclear cell)) has a complete copy of our DNA. That means that every nuclear cell contains a full set of genes for producing proteins and other products.

It is only in certain cells, in certain circumstances, that certain genes are needed to be transcribed (copied to RNA) and translated (copied to amino-acids to make proteins) so that these products are - um - produced.

This is done, not by addressing any specific DNA locations, but by substances being released that chemically interact with special DNA areas called promoters, wherever they happen to be in the DNA. This interaction begins the process of transcription and subsequent translation.

To pick up on the recipe analogy, it's as if a customer has arrived at a restaurant and ordered a soufflé. The waiter conveys the order to the kitchen. The chef calls it out, "Soufflé!" And wherever the soufflé cook happens to be, he or she hears the order being called out and cries, "Yes chef!" and proceeds to crack eggs.

The soufflé gets cooked and served up. In the same way, a DNA-specification of a product (the recipe) gets turned into the product itself. It doesn't matter where the specification is located.

"Syncytin" genes are a good illustration, showing that the position of a transcription unit is irrelevant to its working. Certain retroviruses - HIV is an example - are able to absorb their target cells together into one "super-cell" that contains all the nuclei thus far absorbed. They do this by way of their env (environment) proteins that allowed them to attach to and combine with their initially targeted cell. Certain placental mammals have endogenous retroviruses with env genes that act during pregnancy in exactly the same way, forming a "syncytial layer" as part of the placenta. But different syncytins from different endogenous retroviruses on different chromosomes are used by different placental lineages!

When retroviral genes are found in the same DNA locations in the genomes of different species, it is not because they have to be in the same special location in order to perform any function they may have. They are where they are because of endogenization in a common ancestor.

But how can you rule out design as an explanation?

A flatfish as an example of dumb "design".

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.

Regarding endogenous retroviruses (ERVs), endogenization fits the bill.

'Design' does not.

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

'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.

'Design' fails to explain such a scattergun approach as using integrase to insert retroviral genes into host cells' DNA with no regard as to whether or not they will cause damage.

A common tactic of creationists, writing about ERVs, (see this page) 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 hypotheses, 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.

1. What is reverse transcriptase designed to do?
2. What is integrase designed to do?
3. Why were ERVs designed with a viral codon bias?
4. What is the design purpose of re-transcribable promoters?
5. What were the HERVs that produced the consensus sequence that generated Phoenix designed for?
6. What is the design purpose of both exogenous and endogenous KoRV?
7. If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
8. What is the design purpose of giving some people certain HERVs and not others? See also - More ancient viruses lurk in our DNA than we thought.
9. What is the design purpose of creating different syncytins in different placental lineages?

How could a species survive a massive invasion of retroviruses into its genome?

1. The short answer is, however a species survived, it did. In humans and chimps, for example, there are some 200,000 ERV and ERV fragments, and here we still are. How do we know the ERVs are of retroviral origin? See here.
2. Some individuals in a population will have natural resistance to any given retrovirus. They will reproduce more successfully, conferring their resistance to subsequent generations. As the next retrovirus comes along, the individuals resistant to that will add their resistance to the gene pool.
3. ERVs can actually provide resistance to further retroviral infection.
4. Retroviruses convert their RNA genomes into DNA by a process called reverse transcription, which is very error-prone. Viruses do not need error checking when reverse transcribing, because they reproduce on a massive scale, and they reproduce very rapidly. Indeed this is why they can evolve so rapidly. It follows that a proportion of integrations will not be successful from the point of view of the retrovirus, and will be harmless, and even, rarely, helpful to the host organism. ERVs represent copies of at least harmless integrations, otherwise they would not have entered the germ-line and been reproduced over generations. The harmful ones, of course, would have not been reproduced.
5. The rate at which new ERVs enter the gene-pool of a species and become fixed (present in all members of the species) is difficult to estimate. Being mostly of neutral fitness value, they are subject to mutation and genetic recombination making their structure erode over time and become difficult to identify as ERVs for sure. The oldest identified ERV at the time of writing is perhaps a bovine BoERV1 which is estimated to be 56 - 128 million years old. Let's use a figure of 100 million years just for simplicity. 200,000 endogenizations (where a retrovirus enters the genome and becomes fixed in the population) in 100,000,000 years means one endogenization every 500 years. It doesn't sound as impossible as some creationists try to make out.

How could ERVs survive programmed cell death (apoptosis)?

By using IAPs (inhibitors of apoptosis) and by error-prone reverse transcription

The same retrovirus or ERV has been found in two species that evolutionists say are very distantly related. How is this possible?

This question reveals a misunderstanding of the case for common descent from ERVs. Retroviruses occasionally cross to other species, often distantly related ones, such as from gibbons to koalas. They can also become endogenous in two distantly related species. The presence of the same retroviruses or ERVs is not evidence for common ancestry. It is ERVs in corresponding locations in the DNA of two species that is evidence of common descent - because a bunch of them are highly unlikely (to say the least) to have ended up in corresponding locations, by chance, from independent infections. The only viable explanation is that both species inherited the corresponding ERVs from the same ancestors. Inheritance guarantees corresponding locations. Separate infections do not.

What if we find an ERV in a common location in chimpanzees and gorillas, but not in humans?

The implication of the viral explanation for endogenous retroviruses (ERVs) is that different kinds of creatures, sharing ERVs in corresponding locations, must have inherited those ERVs from common ancestors.

Something that sometimes confuses the issue is a study that identified one ERV, HERV-K-GC1, that is present in chimpanzees, bonobos and gorillas, but not in humans.doi:10.1016/S0960-9822(01)00227-5 How this could be is explained in the paper. This page presents that explanation in a simplified manner.

The scientific consensus is that gorillas split from the common ancestor of all four species, followed by humans, followed by the chimpanzee-bonobo spit.

How, then, could HERV-K-GC1 be inherited from the common ancestor of all four species by gorillas, chimpanzees and bonobos, but not by humans? Surely there is something wrong here? Doesn't this result contradict the science?

Well, in order to be a contradiction, the result would have to be an impossible one, according to the science. So is the result impossible?

Consider what the viral hypothesis says. An ERV is introduced into a population of organisms by the integration of a retrovirus into a single germ-line cell. Offspring descended from that germ-line cell may or may not inherit that ERV. If any offspring do inherit it, and their offspring too, and so on, that ERV will spread among the population. If it eventually spreads to every individual, we say it is fixed in the population, and every subsequent offspring will inherit it. But all the while it is not fixed, there will exist in the population, individuals with the ERV, and individuals without. Of course, the ERV may eventually die out, as opposed to becoming fixed. In this case, it is the pre-intergration allele that becomes fixed once more. Bear in mind that at the time of writing, there is good evidence that chimps and humans share some 200,000 ERVs and ERV remnants. It is hardly out of the question that such exceptional cases can arise.

This all means that individuals, populations or species that descend from a population that has an ERV that is not fixed need not inherit that ERV.

In other words, common ERVs testify to common ancestors, while the absence of a common ERV does not falsify common ancestry. Look up "incomplete lineage sorting". An example - http://biologos.org/blog/understanding-evolution-speciation-and-incomplete-lineage-sorting

Evidence of unfixed (non-ubiquitous) ERVs in the human population can be found @ Long-term reinfection of the human genome by endogenous retroviruses