Does Dr. Andrew Fabich have the worst ERV argument?

For those unfamiliar, Fabich has posted a few articles on AiG where he argues that:

ERVs were created to “provide for the good things in our genome, but the curse may have caused some ERVs to exit the genome and become active outside of cells.”


”As such, some virus genomes (e.g., Ebola) are found within the genome of organisms and in a dormant state. Ultimately, it would be great to have an explanation for the original location within a host genome for every virus like retroviruses or Ebola, but the truth is that we cannot know the original genomic location for every viral genome.”


“Why does the retrovirus have to become part of the host to begin helping as opposed to already having been there and helping from the beginning?”

Essentially, Fabich’s argument is that all or most viruses were part of the genomes of various organisms, before they were corrupted in the fall and “exited” the genome becoming free agents.

Obviously there are a couple problems with this argument:

It doesn’t explain novel viruses. How did Ebola leave its dormant state in the guinea pig genome 6000 years after the fall? A mechanism needs to be described.

It’s also inconsistent with observational science: we observe ERVs inserting their genes into host genomes today. Experimentally, if fixed, dormant ERVs are extracted from host genomes, they can still be infectious.

It is not a falsifiable theory. It relies on supernatural special pleading, and there is no empirical way to test this or make predictions with it.

It seems to clash with christian doctrine. If all animals reproduce after their own kind, how are viruses the reproductive, genetic descendants of other kinds of organisms?

If not all viruses are the result of rogue ERVs after the fall, which viruses are and aren’t? Is there any way to predictably tell? Why did God use an undistinguishable genetic pattern twice in creation, was it just to trick us into believing there is evidence for common ancestry?

I’m writing and recording a video on this theory, and I wanted to know if any with a better understanding of genetics/biomechanics could add any more arguments or explain any concepts that I’m missing. Thanks!


Have you talked to @BarryDesborough (or @Barry_Desborough1) ?? He has written extensively on the topic.

Also, Welcome to Peaceful Science @Andrew_Christianson :slight_smile:


You also have to wonder why “The Fall” would cause viruses to gain the function of transmission between individuals, not to mention transmission between different species. Is the fall like just some sort of radiation that causes mutations?

God curses all living things(?), and then for some completely inexplicable and frankly nonsensical reason that makes them suffer genetic mutations, and these in turn make some molecular systems capable of extracellular and zoonotic transmission?

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I guess this isn’t actually an argument, per se, as a case example of how creationists think science should be done. Not a pretty sight, is it?

I have not! I will read through his posts.

Here is Barry’s Blog, if you haven’t found it already:


Maybe there’s a textual corruption and it should be “fall-out”.

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See also Encyclopedia of American Loons: #1597: Andrew Fabich

Here is my fisk of one of Fabich’s articles. Veritas: Do Endogenous Retroviruses (ERVs) Support Common Ancestry? Yes, they do!


Hi Andrew
I think you may want to explore the fixation issue. The rareness of a viral mutation in a unique position and fixed in the populations genome may not be reconcilable assuming the average mutation is neutral and the rate of occurrence of retroviral infections in the germ line . This will test if the observation is likely a viral infection.

Don’t worry if you can’t make sense of that gobbledygook , @Andrew_Christianson. You’ll soon realize that Bill’s inability to form coherent English sentences is only exceeded by his utter incomprehension of any scientific topic whatsoever. But you likely already realize this.

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@Andrew_Christianson to briefly fill you in on past events, Bill has had this “fixation issue” explained to him many times, yet continues to behave as though this has never happened at all. He assumes that a new variant of an allele can only enable a singe trait, and that trait can have no effect on selection until after it becomes fixed. The fact is that a new allele may contribute to more than one trait, creating combinatorically many potential new/different traits. If a new allele only interacts with 100 other alleles, then there are over 4 million potential traits allowed by the interaction of 5 or fewer allele. Allow 200 other alleles instead of 100, and the number of combinations rises to ~66 million. 1000 other alleles → ~8 trillion 5-way combinations.

I could continue on with the example and even bigger numbers, but that misses the point. Bill only allows for a single function for any new allele, when it’s simple to show how there could be a great many.


Indeed. Bill also appears not to understand epistasis.

This will test if the observation is likely a viral infection.

ERV sequences are near-complete viral genomes, and they can be revived in lab experiments. Are not genetic identity and observed behavior as infectious agents better tests to confirm viral nature?

assuming the average mutation is neutral and the rate of occurrence of retroviral infections in the germ line .

How has the rate of occurrence been calculated? The only method that I am aware of is phylogenetically, but it would be circular to argue that integration rates disagree with phylogenetics since integration rates are based on phylogenetics.


So it seems like his argument is that, if you ignore the processes that govern fixation; natural selection, the founder effect, genetic bottlenecks, genetic drift, etc, then there aren’t enough fixed ERVs?

Sorry for splitting my reply in two, still learning the PS forum. :slight_smile:

assuming the average mutation is neutral

The paper that you private messaged to me mentions this:

solo-LTRs would also be expected to be deleterious, since they contain the retroviral regulatory sequences affecting host gene expression. Our data support this model in terms of fixation.

I believe this contradicts the assumption that the average ERV insertion is neutral in terms of calculating fixation rates, no?

Hi Andrew,

I think that you might want to know that the conditional “can still be infectious” is unnecessary, because I’ve personally experimentally reverted an inactivating mutation in a mouse ERV, restoring infectivity, a mere 32 years ago:

Hi Bill,

You might want to look at what real people really do, instead of producing more word salad.


Something like that. Bill is generally unwilling to commit to any well defined claim.

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Give it an hour or so and it’ll change.

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