ERV Starship

Sounds like job security to me :)

We've known for almost fifty years that bacterial genomes can harbor viruses and we've known for almost forty years that this applies to all kinds of viruses. We've also known that many of those viruses are defective.

It's hard for me to understand why people are making such a fuss about discovering the same thing in animal genomes. Is it because these people thought that animals were going to be fundamentally different than bacteria in spite of what Jacques Monod predicted?

Or is it because we've stopped teaching the basics of prokaryotic molecular biology and the current generation of students doesn't know about bacteriophages lambda and Mu?

Oh, I'd be willing to bet that there are a few functional EVE's from DNA viruses out there somewhere, but I'd also be willing to bet that the vast majority are not functional and never have been.

Finally, if and when we ever do find a functional EVE, I'd be willing to bet it will be used by some people as evidence that all EVE's have function...

LOL!

Its part of the phage/retroviral life-cycle to integrate into their hosts genome. So finding phages/retroviruses permanently integrated into genomes is not surprising.

It is surprising to find other kinds of viruses permanently integrated into their hosts genome, because integration is not a stage in their life-cycle. Each one of these viruses are unexpected for different reasons-- they all lack RT activity, they all lack integrase activity (though nuclear dsDNA viruses will semi-regularly accidentally integrate without integrase, like HPV), some should never have a dsDNA stage of their life-cycle, some should never even be found in the nucleus, and frankly, I cant imagine any of them really wanting to hang out in eggs/sperm.

There is a long series of highly unlikely events that have to take place to integrate these viruses into genomes in the first place, and then we have to add on top of it the odds that the allele gets fixed in the population. We have to assume that this has happened more times than we have evidence for, as some integrations never got fixed in the population, and some made the organism DOA.

I can assure you we learn about lambda :P

So... how the flaming nora do they wind up in DNA? What's the chemistry here?

From a population genetics side, how often must this be happening? And if it's so common then how come we've never caught a non-ERV virus in flagrante delicto?

If we have so many viruses popping into our genes every few generations, how much damage are they causing? Does this have any medical significance?

Too much question. My brain asplode.

Abbie, have you seen the reports of HERV-W in multiple sclerosis patients and, given your expertise, what do you think of the data? There are reports of production of virions in these patients. Or is it just crap like XMRV in autism?

Clinical Reviews in Allergy and Immunology
Volume 39, Number 1, 51-61, DOI: 10.1007/s12016-009-8170-x

Multiple sclerosis and HERV-W/MSRV: a multicentric study. International Journal of Biomedical Science, Vol. 3 (4), p. 292-297, (2007).

Great. Now I feel sick.

ERV,

Interesting that some of these "junk" EVE's have open reading frames. So, in your opinion, would it be conceivable to "Phoenix" any of these EVE's?
http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter

There is at least one known functional endogenous nonretroviral virus in some families. I think it causesd high amounts of cancer in the hosts =\

I was certain that ALL KINDS of cryptic viral DNA can be found in bacterial genomes including all those bacteriophage whose life cycle never requires integration (e.g., T4 and T7 in E. coil). However, I was unable to come up with a good reference after a quick search so I may be wrong.

Given that all cells contain active recombination enzymes it's almost certain that some pieces of viral DNA (or RNA) will eventually find their way into the host genome by accident. This might be more evident in eukaryotes since they have bigger genomes and can tolerate more junk DNA.

Glad to hear that you've learned about lambda and Mu (and P1, T4, etc.?), Abbie. Do most of your fellow students know about prokaryotic molecular biology?

Larry--

I cant speak for other departments, but the micro-immuno curriculum was split up into ~50% immunology, 35% bacteria (including phage), 15% protists/fungi/viruses.

Because Im at a med school instead of a regular uni, we focused on pathogens that cause human disease-- integrated phages are often virulence factors, so we did go over them in a lot of detail. Archaea we never touched. I only know about them as a novelty-- their viruses are cool (viruses surviving in boiling acid pools=cool).

No clue what other depts do, though!

Ehh color me not surprised, but then I work in a Molecular Fossil Lab. As for the molecular basis of it look at the early recombination studies where a plasmid with an interrupted region of homology could be either integrated or 'repaired', or the fungal mt plasmids some of which pick up a region of homology and then integrate.

The medical oriented departments have a different approach than those of us in basic research. The hyothesis that viruses are derived from the host genome tends to take a lot more weight to them than the hyp that these are remnants from the RNA or early DNA worlds.

Sequence similarity can indicate shared ancestry but it cannot tell which direction the DNA travelled if horizontal transfer is suggested. We can't say whether a virus picked up a bit of DNA from vertebrates, or if it deposited a bit of its DNA into vertebrates unless there is quite high similarity and other clues (such as finding a complete or nearly complete viral genome in one branch of vertebrates that is lacking in the surrounding branches).

For example, with the "CERV-1" and "CERV-2" Chimpanzee endogenous retroviruses, at least some copies of them have LTR-Gag-Pol-Env-LTR full genomes, and they are found only in a few primate species and lacking in others (such as human genome) in a way that makes it clear that chimpanzees picked up this ERV rather than humans having lost this ERV.

Some of the other alleged "endogenous virus" sequences are not at all that clear. The sequences with similarity to the virus are found in all species and that similarity is so low that it is not at all clear when or how the similarity was shared. All DNA polymerases for example share some similarities, as do all reverse transcriptases.

I reiterate my previous observation that "ERV Starship grumblegrumble" would be a fantastic name for a Blog.

"There is no way. There is just no way, man, for Creationists to deal with this"

Yeah, great news indeed...

First of all there is the RNA virus paradox. It says all RNA viruses, and their socalled remnants ERVs, have a common ancestor around 50 thousand years BP.

Still, ERVs are present in all known animals, which are allegedly millions and million years apart...a paradox.

Close-up scrutiny of ERVs reveals unexpected surprises. For instance, some found in coelecant and humans have the same unique features. Evolution? Common descent? Apparently not...

Could it be that main stream scientists are wrong about their interpretation that ERVs are the ancient remnants of RNA viruses? Regarding the above facts, most probably YES.

What can an ERV be then? If anything?

Could it be that ERVs (containing gag and pol only) were designed as variation-inducing genetic elements (VIGEs)? Could it be they were controlled and regulated in the past, but due to their redundant character easily degenerate into junk DNA?

The origin of RNA viruses (gag & pol plus additional genes) is currenlty completely obscure. There is not a single scientist in the entire world who can tell you an plausible origin story, where RNA viruses have their origin...

Could it be that RNA viruses (such as HIV, Flue, RSV, etc) have their origin in VIGEs?

Could that be the case? Do Darwinians mix up cause and result?

Yes, that is moste likely the case.

RSV is a "simple" RNA virus that is able to cause carcomas (cancer). If we study the genetic components of RSV we observe again gag and pol. In addition, we vind part of a gene we know as src. This gene is a cell cycle control gene we find in all higher organisms, and itposseses a molecular on-switch and an off-switch.

Now look how RSV originated: The VIGE integrated near the SRC genen, and when it excised it accidentally picked up only the on-switch of the SRC gene. The births of an ocogene!

This is how all RNA viruses arose: from VIGEs.

Why is it plausible? Because this view solves the RNA virus paradox. And it explains RNA-virus-caused diseases as secondary.

Have a nice day,

Peter Borger, PhD
Biologist

PS: Humans and chims differ by hundreds of unique genes, including protein coding- and miRNA genes. As long as Darwinians don't have a clue about such novelties, the independent integration of ERVs and the like, in specific sites in the genomes of primates, explains why they give an illusion of common descent. Mutations are not a random phenomenon, guys. For more information read my articles in the JOC.

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First of all there is the RNA virus paradox. It says all RNA viruses, and their socalled remnants ERVs, have a common ancestor around 50 thousand years BP.

Wrong. What it actually says is that for any given RNA virus family, the actively circulating viruses diverged from a common ancestor less than 50,000 years ago according to an assumption of a constant molecular clock. The same clock shows that the RNA virus families diverged from each other so long ago that the clock is useless. It absolutely does not say that "all RNA viruses...have a common ancestor around 50 thousand years BP."

Actually, let me restate that a bit. What is happening is that the molecular clock used can't determine divergence for anything over 50,000 years old. That is for something with a genome of this size and an assumed constant mutation rate. It turns out that most RNA viruses within a family have divergence times that can be determined by the clock. But...

RNA virus families are determined by genetic similarity! Anything too dissimilar to reliably estimate divergence is put in a different family.

(This all comes about because RNA viruses have no repair mechanisms to slow down the mutation rate. Most life does have repair mechanisms, so molecular clocks are capable of semi-reliable dating for much longer periods of time. It's kinda like the difference between carbon dating and uranium-lead dating)

No need to change the blog's name - just change what ERV stands for! Extremely Radical Viruses, say.

Listen, guys, and listen carefully...

Where do RNA viruses have their origin?

Excacty! In the genomes of living organisms.

They have thier origin in variation-inducing genetic elements. VIGEs!

Darwinians have turned biology up-side-down. Let's turn it down-side-up-

GUToB!

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