Creationist ERV Misinformation

Proposed forum: Human Evolution and OriginsThe purpose of this thread is to catalog the misinformation creationists have put out on the internet regarding endogenous retroviruses (ERV's).Let's start with the facts.First, a bit of terminology. An orthologous feature is a feature found at the same base in two genomes. Therefore, an orthologous ERV is a viral insertion found at the same base in two genomes. If they are not found at the same base then they are non-orthologous.The 2001 human genome paper found 203,000 ERV class I-III insertions comprising 4.64% of the human genome. An additional 3.65% of the human genome is comprised of MaLR's which are retroviral terminal repeats that have combined with a transposon. It would be correct to say that MaLR's have viral sequence, but they aren't the product of viral insertion so I usually don't count them as being the same as ERV's. Here is table 11 from the 2001 human genome paper.
Initial sequencing and analysis of the human genome | NatureThe 2005 chimp genome paper mapped all of the ERV's in the chimp genome and compared them to the human genome. They reported the lineage specific ERV's for both chimps and humans which are the non-orthologous ERV's. By default, the rest are orthologous ERV's. In table 2 of the chimp genome paper they report 82 human specific ERV's and 279 chimp specific ERV's. These again are the non-orthologous ERV's. This means that out of the 203,000 ERV's reported in the human genome only 82 are not shared with chimps at the same base.
Initial sequence of the chimpanzee genome and comparison with the human genome | NatureThat is where we are starting from. If a creationist source tries to tell you differently then they are misinforming you about the number of orthologous ERV's.This one piece of information will cover a lot of the misinformation creationists are trying to pass off on their audience. Future posts will cover some of these examples.

The first example comes from the Discovery Institute. Do Shared ERVs Support Common Descent?I think I may cover quite a few pieces of misinformation from that article, but for now I will focus on one of the main bits.

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Out of tens of thousands of ERV elements in the human genome, roughly how many are known to occupy the same sites in humans and chimpanzees? According to this Talk-Origins article, at least seven. Let’s call it less than a dozen. Given the sheer number of these retroviruses in our genome (literally tens of thousands), and accounting for the evidence of integration preferences and site biases which I have documented above, what are the odds of finding a handful of ERV elements which have independently inserted themselves into the same locus?

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This article was written in 2011. This is 6 years after the chimp genome paper was written. As discussed in the opening post, the chimp genome paper reported that more than 99% of the 203,000 ERVs in the human genome are shared with chimps at the same base in each genome. There aren't fewer than a dozen out of 10's of thousands of ERVs. There are only 82 that aren't shared out of 203,000.This completely destroys the main argument of the Discovery Institute article. They were trying to claim that due to preferential targeting of DNA sequence motifs that you would expect a dozen or so insertions to be the same if they were independent insertions. If that is their expectation, then they simply can't explain how more than 99% of 203,000 insertions are found at the same base.

An initial search doesn't turn up anything specific about the 82 identified in the chimp genome paper. However, there are many papers on HERV-K insertions themselves which is the family of ERV that most of those 82 fall into.Since these are lineage specific insertions we would predict that they inserted close to the split between our lineage and the chimp lineage and after the split. Therefore, they should be young insertions.What would we expect from young insertions? We would expect that far fewer mutations have accumulated in these sequences compared to older insertions. We may also find that some are polymorphic since they haven't had time to become fixed. That is, we may find individuals who are heterozygous for the insertion, having both the ERV and the untouched pre-integration site.Is that what we see with HERV-K? Yep, sure is.

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HERV-K (HML-2) is the only group of HERV-K containing human-specific and polymorphic loci. Polymorphic loci that are unfixed in the modern human population suggest that they remained transcriptionally active up to very recent times in the evolutionary history of the Homo Sapiens species. When compared with other HERV loci, HERV-K (HML-2) have fewer accumulated mutations, indicating that they likely continue to co-evolve with the host, and they are probably still biologically active at present. Insertionally polymorphic HERV-K (HML-2) loci show different structural features, including full-length provirus integration, solo-LTR integration and unoccupied pre-integration, in different individuals [11, 12]. [emphasis mine]
Identification of the distribution of human endogenous retroviruses K (HML-2) by PCR-based target enrichment sequencing | Retrovirology | Full Text

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Continuing with the misinformation from the Discovery Institute article in message 4.The author makes this misinformed claim:

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In one relevant study, Barbulescu et al. (2001) report that,

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We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome. Humans contain an intact preintegration site at this locus. [emphasis added]

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It seems that the most plausible explanation for this is an independent insert in the gorilla and chimpanzee lineages. Notice that the intact preintegration site at the pertinent locus in humans precludes the possibility of the HERV-K provirus having been inserted into the genome of the common ancestor of humans, chimpanzees and gorillas, and subsequently lost from the human genome by processes of genetic recombination. Though there are other possible candidate hypotheses for this observation (such as incomplete lineage sorting), in the context of other indications of locus-specific site preference, this data is, at the very least, suggestive that these inserts may in fact be independent events.

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The author almost got it right. The most probable explanation is incomplete lineage sorting (ILS). About 30% of the human genome is more similar to gorillas than it is to chimps due primarily to ILS. It isn't surprising that polymorphic ERVs would be amongst that 30%.What is ILS. It's pretty simple, actually. Primate genomes are diploid, so we have two copies for each section of DNA which are called alleles. An ERV is an allele like any other. As seen with human specific HERV-K insertions, ERVs can be insertionally polymorphic meaning people can have one copy of the pre-integration site and one ERV allele. After a speciation event the ERV alleles can remain polymorphic, and in some lineages the ERV may fix and in others the pre-integration site may fix.Why the author thinks two independent insertions is more probable is a bit baffling given the widespread ILS observed in the trio of gorilla, chimp, and human.

Continuing the discussion on the Discovery Institute article from message 4.This next section is a bit of a mixed bag. I will discuss after the quote.

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Another study, by Sverdlov (1998) reports,

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But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified ‘hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically. [emphasis added]

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I could continue in a similar vein for some time.

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To be fair, if we are very, very generous the math that follows will fall in line with the author's claim that out of tens of thousands of insertions we may expect a handful of orthologous ERVs to be the product of independent insertions. However, this citation is used a lot by creationists to pretend as if the actual state of orthologous ERV's (99+% of 203,000 ERVs) can be explained by this paper. Well, it can't.The cited paper is not the actual primary source. It was only referencing another paper in the introduction.

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Ty transposons reflect important properties of their viral relatives, striving for transcriptionally active regions to insert their cDNA copies [37]. This is not surprising considering that the retroviral genes integrated in the genome need the host transcriptional machinery to express themselves. But although this concept of retrovirus selectivity is currently prevailing [37], practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified `hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically 41, 43.
https://www.sciencedirect.com/...ticle/pii/S0014579398004785

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So let's go to the primary source.

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In all experiments, estimates of the m.o.i. ranged from two to three integrated proviruses per cell. A pool of 10 ug of infected TEF DNA (from ~5x l0^6 cells) would therefore contain ~1-1.5 x 10^7 integration events. If integration occurred at random throughout the genome (size 2x 10^9 bp) we would expect to see about two to three integrations, in each orientation, within the 500-bp stretch of DNA analyzed in each reaction.
Withers-Ward et. al, 1994

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Let's go with 1E7 integration events to keep the math simple. 1E7 insertions across 2E9 bases 1 integration every 200 bases, so about 2 to 3 insertions per 500 bases as the paper states. They are counting both strands, so the math makes sense.If insertions were truly random, what would we expect from 2E5 insertions (i.e. 200,000 human and chimp ERVs)? We would expect an insertion every 10,000 bases. This gives a 1 in 10,000 chance of two independent insertions occurring at the same base. For 200,000 ERVs, this would be about 20 insertions, far short of what is seen. If we assume that the entire genome is made up of the preferred DNA motif for retroviral insertion (which it isn't, but just for the sake of argument) we would see 5,600 insertions at the same spot due to independent insertions. Again, far, far short of 99% of 200,000 ERVs seen in the real data.There is also another set of criteria that are important here. Not only are the viral insertions at the same spot, but they are also the same viral sequence (plus mutations that have occurred since the human and chimp lineages split). It's not as if two different viruses inserted at the same base. It's the same virus, and there are many, many different types of viruses that comprise all ERVs.So our real probabilities should be for the same virus hitting the same base. Those probabilities quickly skyrocket. Just from my reading, I think it would be generous to say that a specific subfamily of retrovirus could produce 1,000 insertions. At 1,000 insertions, the odds of that specific retrovirus producing the same insertion at the same base in two independent events would be 1E3 in 2E9, or 1 in 2 million. In other words, not likely at all for 200,000 insertions.So if you see a creationist citing this paper, know that they are blowing smoke. The math just doesn't add up for them.

Continuing discussion on the Discovery Institute article from message 4.Another common piece of creationist misinformation on ERVs is found in this same article.

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In addition,Yohn et al. (2005) report that,

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Horizontal transmissions between species have been proposed, but little evidence exists for such events in the human/great ape lineage of evolution. Based on analysis of finished BAC chimpanzee genome sequence, we characterize a retroviral element (Pan troglodytes endogenous retrovirus 1 [PTERV1]) that has become integrated in the germline of African great ape and Old World monkey species but is absent from humans and Asian ape genomes.

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Creationists often try to pass this off as an example of ERVs that violate the expected distribution. In fact, this is a perfect moment to contrast the two sides.Creationists: Orthologous ERVs are due to similar viruses inserting into similar sequence independently of one another.Evolutionists: Due to the random nature of retroviral insertion, the chances of independent insertions happening at the same base is highly improbable. The best explanation is a single insertion into a common ancestral genome.So let's test these arguments using PtERV1 insertions. The evolutionary prediction would be that these insertions happened after the split between the chimp/human branch and the gorilla branch because the insertions are not found in the human genome. In addition, PtERV1 insertions can be found in the macaque genome, but not in the orangutan genome. Again, this leads to the conclusion that these germline invasions occurred very recently. Therefore, there should be few, if any, insertions at the same base in the chimp, gorilla, and macaque genomes. The creationist prediction is that we should see the same rate of orthology in the PtERV1 insertions that see for ERVs overall in the human and chimp genomes.So which is right? Let's go to the Yohn et al. (2005) paper and find out.

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In addition, we used BAC end sequences from nonhuman primate clones harboring full-length retroviruses to map their locations back to the human genome. We then compared the locations (Figure 3; Table 2) between species to determine whether the sites were non-orthologous. Based on an analysis of 1,467 large-insert clones, we mapped 299 retroviral insertion sites among the four species (Figure 3; Table S2). A total of 275 of the insertion sites mapped unambiguously to non-orthologous locations (Table 2), indicating that the vast majority of elements were lineage-specific (i.e., they emerged after the divergence of gorilla/chimpanzee and macaque/baboon from their common ancestor).

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Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous (Table S3). We classified these as “ambiguous” overlap loci (Figure 3). If all 24 locations corresponded to insertions that were orthologous for each pair, this would correspond to a maximum of 12 orthologous loci. The number of non-orthologous loci was calculated as 275/287 (275 + 12) or 95.8%. This is almost certainly a lower-bound estimate owing to the limitation of our BAC-based mapping approach to refine the precise locations of the insertions.
Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans - PMC

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First, the title of the paper should give it away. These are lineage specific insertions. But hey, when have creationists ever been scared away by a paper whose title completely refutes their argument from the get go. With that said, let's move on.They were able to map 299 insertions, of which 275 were unambiguously non-orthologous based on BAC end sequencing. Overall, ~96% were unambiguously non-orthologous. That's a far cry from the less than 1% of ERVs that are non-orthologous in the human and chimp genomes.The 12 possible pairs that remain are ambiguously orthologous because of the method they are using, which is BAC end sequencing. In this method you break up the genome into big chunks, about 160,000 base pairs in the case of the Yohn et al. paper. This allows them to say that there is a viral insertion somewhere in that 160,000 base pairs, but they can't determine exactly where the insertion is within that big chunk of DNA. Since they can't map the insertion to a specific base it could be orthologous, but it could also be non-orthologous. You need 1 base resolution in order to know.At the time of their publication there weren't high quality assembled sequence for different primate genomes, so they were limited in what they were able to compare at 1 base resolution. However, they were able to rule out some additional ERVs as being orthologous:

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For the three intervals putatively shared between macaque and chimpanzee, we attempted to refine the precise position of the insertions by taking advantage of the available whole-genome shotgun sequences for these two genomes. For each of the three loci, we mapped the precise insertion site in the chimpanzee and then examined the corresponding site in macaque (National Center for Biotechnology Information). In one case, we were unable to refine the map interval owing to the presence of repetitive rich sequences within the interval. In two cases, we were able to refine the map location to single basepair resolution (Figures S4 and S5). Based on this analysis, we determined that the sites were not orthologous between chimpanzee and macaque. . . Although the status of the remaining overlapping sites is unknown, these data resolve four additional sites as independent insertion events and suggest that the remainder may similarly be non-orthologous.

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So the authors concluded that the bulk of PtERV1 insertions are no orthologous, and they don't expect the remaining ones to be orthologous.So why do creationists keep citing this paper? It completely destroys their argument. It is a perfect example of twisting science to say the exact opposite of what it actually says, and then feeding it to an unsuspecting audience.BONUS:Further analysis has been done on PtERV1.

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Endogenous retroelements are among the longest retrotransposons within mammalian genomes (up to 10 kbp) and are frequently misassembled because of their copy number and sequence identity. The chimpanzee and gorilla lineages carry an endogenous retrovirus, PtERV1, that is absent in orangutan and human genomes (29, 30). None of the PtERV1 integrations between chimpanzees and gorillas appear orthologous, suggesting independent retroviral integrations in these two lineages (29, 30) or that humans and orangutans contain extrinsic factors that differentially restricted propagation (31). A high-quality map of 540 PtERV1 elements (both full-length and solo long terminal repeat [LTR]) in chimpanzee and gorilla (Table S7) (16) shows that their integration events are nonorthologous (99.8%), biased against genes, and integrated in the antisense orientation (Figs. S30, S31) consistent with the action of purifying selection.

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Using the more complete ape genomes, we identified only one chimpanzee–gorilla orthologous PtERV1 element, not present in modern humans, that was lost through incomplete lineage sorting and integrated roughly 4.7 mya (95% HPD: [1.9, 7.2 mya]; Fig. 2e). We named this element the “source PtERV1” as it was present in the common ancestor of all African apes and was likely the progenitor for independent expansions to non-orthologous loci in the chimpanzee and gorilla genomes. The source PtERV1 was likely missed in earlier genomic studies of draft genomes because the locus (sharing orthology with human chromosome 19) (16) is repeat-rich and the integration site is an ancient LTR element.

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High-resolution comparative analysis of great ape genomes - PMC

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They were able to map even more PtERV1 insertions, and they were non-orthologous, except for 1. It was dated to about 4.7 million years ago, right at the point where the human and chimp lineages diverged. It is thought that humans lost this ERV through incomplete lineage sorting (also discussed in a post above this one).Again, this all fits with the predictions made by evolutionary theory, but they are in stark contrast to the predictions made by the creationist model.

On the Venn diagram of creationist arguments there is an overlap between junk DNA and ERVs, so I will address some of those arguments here.The ERV evidence for common descent does not require ERVs to be junk DNA. Even if all ERVs were functional they would still be evidence for common descent because of the pattern of distribution for orthologous ERVs and their sequence divergence. Scientists have concluded that the vast majority of ERVs are junk because of many pieces of evidence, including the fact that the vast majority of ERVs accumulate mutations at a rate consistent with junk DNA.Just to stress this, the conclusion is that the VAST MAJORITY of ERVs are junk. For example, this paper:

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The genomes of modern humans are riddled with thousands of endogenous retroviruses (HERVs), the proviral remnants of ancient viral infections of the primate lineage. Most HERVs are nonfunctional, selectively neutral loci.
Just a moment...

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So, it's a bit like this:Evolutionist: The vast majority of ERVs are junk DNA.
Creationists: You're wrong because scientists found function in a few hundred ERVs out of the 200,000 ERVs in the human genome.
Evolutionist: *insert Star Trek facepalm meme*A specific example can be found here:

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Viruses and immunity are hot topics these days, and a new article in the Journal of Virology, “Switching Sides: How Endogenous Retroviruses Protect Us from Viral Infections,” has the potential to be a paradigm-shifter on the standard view that endogenous retroviruses (ERVs) are junk DNA.
Junk No Longer: ERVs Are “Integral” and “Important Components” of Immune Responses | Evolution News

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Once you chase their citations to the primary literature, you arrive at this paper:Just a moment...A very quick synopsis is that the authors found ERVs whose expression was upregulated by infection with influenza, and those ERVs were important for reducing the impact of the infection.Let's look at one of the figures from the paper:This figure shows the number of ERVs and other repetitive elements that were upregulated or downregulated by influenza. They tested a few gene knockouts and variables, but the takeaway for this thread is that they were only able to find less than 100 ERV elements whose expression was modified by influenza.So less than 100 ERVs were demonstrated to be functional in this paper. Does this refute the finding that the vast majority of the 200,000 ERVs in the human genome are junk DNA? Obviously not.

"Know" and "proof" run into the same sort of language and philosophical problems in science. When a scientist says that they know something or that something is proven they tacitly attach "beyond a reasonable doubt" to the end of it. So with that caveat . . .The conclusion that DNA is junk is based on evidence. One of the primary pieces of evidence is sequence conservation. The basic assumption is that if a sequence is accumulating mutations at a rate consistent with neutral drift then it probably lacks function. If there is function then deleterious mutations would occur, so the lack of selection against deleterious mutations is evidence for lack of function.It is also important to differentiate between "does something" and "has function". To use an analogy, the garbage in your kitchen trash can releases odor molecules into the air. It does something. However, it's still junk. DNA can take part in different molecular reactions, be transcribed into RNA, and even be translated into protein and still be junk. Yes and no. There may be sections of DNA where the sequence doesn't matter but the spacing does. So a sequence can be anything, but the physical distance it puts between two other features may matter.At the same time, nature has already run this experiment in some species. One great example is the bladderwort, a carnivorous plant that lives in nutrient poor environments. It's genome has about the same gene count and gene content as other plant species, but its genome is a tiny 0.082 billion base pairs (Gbp). This is in comparison to other related plants that have genomes in the hundreds of millions to many billions of bases. Evolution has essentially stripped the bladderwort genome of nearly all of its junk DNA. It is thought that more than 95% of the bladderwort genome is functional.Another example is an experiment where they removed millions of bases of junk DNA from the mouse genome, and the mice were identical to their peers after the deletion.Megabase deletions of gene deserts result in viable mice - PubMedYet another example is the lack of introns in nearly all genes in the brewer's yeast genome. Dark matter is a so-so analogy. The name dark matter is used to because dark matter does not emit light. However, its presence can still be detected by its gravitational effects. We can see junk DNA, and it behaves like junk DNA (i.e. it is subject to neutral drift) just like dark matter behaves like matter. It is entirely possible that there is a fraction of what we consider junk DNA that is actually functional, but no one expects it to be a significant fraction. It all keeps coming back to sequence conservation. As Dan Graur put it in response to the ENCODE paper from a few years back:

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Thus, according to the ENCODE Consortium, a biological function can be maintained indefinitely without selection, which implies that at least 80 − 10 = 70% of the genome is perfectly invulnerable to deleterious mutations, either because no mutation can ever occur in these “functional” regions or because no mutation in these regions can ever be deleterious. This absurd conclusion was reached through various means, . . .
https://academic.oup.com/gbe/article/5/3/578/583411

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He then goes on to describe why ENCODE should not have claimed there was function in ~80% of the genome.

It is also worth mentioning that there is no ideological or philosophical reason why scientists need genomes to be full of junk DNA. As noted earlier, scientists were ecstatic when they found a plant genome that was almost entirely functional, and they were happy to delve into the evolutionary history of that genome. Many bacterial genomes have very little junk DNA, and many viral genomes barely have any junk DNA at all. These all fit just fine into the theory of evolution.It just so happens that there is mountains of evidence that about 90% of the human genome is junk DNA. It's the evidence that led scientists to those conclusions.In case people want some not light reading, this paper might be worth the time:

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From extrapolations we estimate that 8.2% (7.1–9.2%) of the human genome is presently subject to negative selection and thus is likely to be functional, while only 2.2% has maintained constraint in both human and mouse since these species diverged. These results reveal that the evolutionary history of the human genome has been highly dynamic, particularly for its noncoding yet biologically functional fraction.
8.2% of the Human genome is constrained: variation in rates of turnover across functional element classes in the human lineage - PubMed

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Returning again to the Discovery Institute's misleading article on ERV's.The article in question was actually a Part 2. Here is a snippet from Part 1:

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One common argument for common descent which one hears very frequently in the evolutionary literature concerns the placement of endogenous retroviruses (ERVs) in orthologous loci in primate genomes. By far the most clear and succinct presentation of the strongest version of this argument which I have encountered can be found in this popular-level internet article.

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That popular-level internet article is this one:Just a moment...The author of popular-level internet article actually responded to the Discover Institute. This bit is most interesting:

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Thus, right from the start, we know that the majority of ERV are in orthologous loci. Here is the summary I gave (for more information, refer to the main page):

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In summary, indel variation shows that most transposable elements, such as ERVs, cannot be lineage-specific; they must be in identical loci. When the indels are examined, this is corroborated, and less than 0.1% of ERVs are found to be lineage-specific (Polavarapu, Bowen, & McDonald, 2006). Finally, definitive confirmation is obtained by genome-wide comparison, where virtually all ERVs are directly observed to be in identical loci (Chimpanzee Sequencing and Analysis Consortium, 2005).

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I want to be very clear; since all indications are that retroviruses began endogenizing tens of millions of years ago (Hughes and Coffin, 2005), common ancestry indicates that the majority of ERVs in the human and chimpanzee genomes must be shared.

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When the author of the DI wrote the article he was responding to a webpage that in no uncertain terms stated that less than 0.1% of the 200,000 ERVs in the human genome were lineage specific, meaning nearly all of the 200,000 ERVs are orthologous.There's no excuse here, and there is certainly no excuse for keeping this article on the DI's website without correction or removal.

I went to the Reasons to Believe website and searched their articles with the keywords "endogenous retroviruses". From what I can see, they all discuss the same misinformation already covered earlier in this thread.You searched for endogenous retroviruses - Reasons to Believe1. Retroviral insertion is not random enough. That's false. Even in a best case scenario, insertional bias will only produce ~1% shared ERV's.2. ERV's have function. Only a tiny fraction can be shown to have function, and even if they all had function they would still be smoking gun evidence for common ancestry.3. PtERV1 is found in chimps and gorillas but not humans or orangutans. They forget to mention that they are not at orthologous positions in the chimp and gorilla genomes.4. Departures from the expected phylogeny. There are known mechanisms that create these departures, such as ILS. It is expected that we will see a noisy phylogenetic signal if species evolved from a common ancestor. It is the ratio of noise to signal that matters, and they are reticent to even acknowledge the massive and overwhelming phylogenetic signal that sits out way above the noise.5. Retroviruses can't produce ERVs in the first place. They acknowledge the case of ERVs being produced by an exogenous retrovirus in koalas, but they tell their audience to just ignore it for no apparent reason.Nothing really original here. Just a rehash of what other creationist authors have written.

I ran across an article at ICR that made a claim about ERV's that I had not come across before:

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First, genetic data indicate that these sequences are not millions of years old. Using the comparative tools of evolutionary genetics, secular scientists compared the gene sequences of viruses to their counterparts in animal genomes and found that, at most, the variation in these sequences indicates they can be no more than 50,000 years old.2 So, if these viral-like sequences are not millions of years old, then where did they come from?

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[off topic note: the use of "secular scientist" still makes me giggle. What's next? Secular baseball players? Secular dentists?]That's a bit convoluted, but their claim is pretty clear. They are claiming that ERVs are not older than 50,000 years. To support this claim, they cite: Molecular Clocks and the Puzzle of RNA Virus OriginsSo what does the paper actually say?

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Although the ultimate origins of RNA viruses are uncertain, it seems reasonable to assume that these infectious agents have a long evolutionary history, appearing with, or perhaps before, the first cellular life-forms (38). While the RNA viruses we see today may not date back quite this far, the evidence that some DNA viruses have evolved with their vertebrate hosts over many millions of years (24) makes an equally ancient history for RNA viruses a natural expectation. Yet a very different picture of RNA virus origins is painted if their gene sequences are compared; by using the best estimates for rates of evolutionary change (nucleotide substitution) and assuming an approximate molecular clock (21, 33), it can be inferred that the families of RNA viruses circulating today could only have appeared very recently, probably not more than about 50,000 years ago. Hence, if evolutionary rates are accurate and relatively constant, present-day RNA viruses may have originated more recently than our own species.

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Well, that's a very different picture than the one painted by ICR. The scientific paper is saying that currently circulating RNA viruses originated no more than 50,000 years ago. It says nothing about ERVs originating within the last 50,000 years. On top of that, the article clearly states that there are examples of DNA viruses that have evidence for host/virus co-evolution over the last several million years. Strange that they didn't mention that (sarcasm implied). The paper also goes on to explain why comparison of circulating RNA viruses leads to these conclusions.The rest of the ICR article hits the usual misinformation bullet points, such as some ERVs having function and no examples of extant exogenous retroviruses producing heritable endogenous retroviruses (see Koala Retrovirus [KoRV]).

Yes. ERV's are either orthologous or lineage specific. If they aren't lineage specific then they are orthologous. If only 82 human ERV's are lineage specific then the rest must be orthologous. The 203,000 human ERV's counted by the Human Genome Consortium was done by top scientists, so I see no reason to doubt it. They used several filters to narrow the field down which means they excluded a lot of ERV's from the study. They were looking for more recent insertions that are full length, so right away they are excluding about 90% of ERV's that are solo LTR's. Of the candidates, they further excluded older full length ERV's because they were focused on more recent insertions, as stated in the results section:

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We wanted to see if recently integrated proviruses accumulated mutations more quickly than neighbouring DNA. Our approach was to examine substitutions into ERVs and their neighbouring genomic sequence that lead to differences between human and chimpanzee. To achieve this goal we identified ERVs and their flanking DNA from both species.
Orthologous endogenous retroviruses exhibit directional selection since the chimp-human split - PMC

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They were NOT trying to measure the total number of ERV's in the human or chimp genome.

Is there anything you would like to see addressed that hasn't been so far?

Do you know of any creationist sources whose articles on ERV's are honest and consistent with the scientific literature? I have yet to find one.