How do retroviruses get into the germ line?

[bascule]

So we have a genome filled with endogenous retroviruses:

 

http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter

 

My question is: how do they infect the germ line?

[Mr Skeptic]

Wow! An 8 pager about retroviruses and their role in our evolution.

 

Retroviruses are quite fascinating, and are used to insert genes in genetic engineering. I've even heard that they can be used to revert adult cells to stem cells. Regardless, they may soon play a much greater role in our "evolution" than they have ever before.

 

...

The prospect of reviving ancient viruses seems like a dangerous idea. Especially if they are able to affect multiple species linked by a common ancestor who originally got the virus (ie, was susceptible). I do anticipate any medical advances they may gain through this, but they had best be careful. I'm particularly interested in the role retroviruses may have in cancer.

[iNow]

http://www.newyorker.com/reporting/2007/12/03/071203fa_fact_specter

 

Thanks for the link. That was a good read.

[bascule]

Well, glad you people enjoyed the article, but..

 

No responses to the OP?

 

Whatever happened to Mokele?

[Skye]

By infecting the germ line cells (eggs and sperm). Only certain retroviruses do this, and they have to be lucky enough to infect the cells that get passed on.

[Mr Skeptic]

By infecting the germ line cells (eggs and sperm). Only certain retroviruses do this, and they have to be lucky enough to infect the cells that get passed on.

 

That, and they have to not be fatal to the resulting fetus. During prenatal development, genetic damage that would not harm an adult much would be fatal to the developing baby. So it has to infect the germ cell in a non-fatal place.

[vampares]

I read all the way through that article yesterday and I can't remember the first thing about it today. Oh well.

 

I found LRE1 the L1.2 LINE RETROTRANSPOSABLE ELEMENT when searching OMIM for retrotransposons. The NCBI map only gestures at the notion; there is no sequence, phenotype or morbidity linked to it.

Hot L1s account for the bulk of retrotransposition in the human population

 

It is almost a functional or it is a functional gene/protien/mutation. This is not clear.

 

There is discusion about the trunctation of the 5' end. This truncated or broken LINE is then transposed and this causes "mutation"/disfunction? Again I don't have a LINE-1 sequence as with every most other genes.

 

There are LINE's discussed as x many in the genome, y are truncated, z are not. There is then discussion about ethnic sampling and further differences which, again, is too abstract for my objective mind.

 

There is also an evolutionary model!

The successive emergence and amplification of distinct Ta L1 subfamilies shows that L1 evolution has been as active in recent human history as it has been found to be for rodent L1 families. In addition, Ta-1 elements have been accumulating in humans at about the same rate per generation as recently evolved active rodent L1 subfamilies.

 

Unfortunately evolving into a tumor is a possibility.

Human LINE-1 retrotransposon induces DNA damage and apoptosis in cancer cells

 

This 22q11.1-q11.2 locus is linked with "Asymmetric crying facies velo-cardio-facial"/DiGeorge syndrome. Which from my understanding looks, ironically like Barbara Bush

 

Do we just watch her and see what develops?

 

I can't determine where the retrovirus's are in the genome. I would not recognize one unless it was designated as one.

[blike]

Mokele is in the jungle somewhere, I presume.

[vampares]

OK if I search "retroviral" I get more hits, like the first half of the long end of chromosome 18. At least they separate p from q.

 

The viruses appear to be confined on the given chromosomes. (?)

 

HERVies are different from L1 and ALU repeats. But they are very similar.

Another DiGeorge's protein, this one a copy of the another one with minor changes. This "duplication" is done pre-human (everyone has this change).

 

"A full-length HERV-K provirus integrated into the low-copy repeat region containing DGCR6, but not to the region containing DGCR6L, after the divergence of chimpanzees and humans. Edelmann et al. (2001) concluded that there has been selective evolutionary pressure toward the functional maintenance of both paralogs."

 

Provirus. Everything about 610524 is a love song. Back in those days everything was simpler and more confused. . .

 

----

 

My HIV/AIDS thread has moved to the outskirts of Limoges. I think it's making for the coast.

 

It is a relevant tie in though, as I think it should be. Relevant that is. The thing is real.

 

The name "retrovirus" however was probably a misnomer. I don't know exactly when HTLV was designated or theorized a "retrovirus". Yet it behaves much like an endogenous retrovirus.

 

Here we have merely tacked the word "endogenous" onto retrovirus. "Endogenous retrovirus" isn't even hyphenated.

 

It calls into question the notion of "pathogen".

 

We have a "polio receptor", a polio virus and a polio vaccine. Not to mention a disease that looks an awful lot like rickets.

 

Who hasn't gotten the flu before? Is the flu endogenous? Viruses are not likely a fantastic bacteria that is so elusive we can only study the nuances from one to the next.

 

So what is viral? We have a virus model.

Can we apply this to retroviruses? RNA/transcripterase is probably all you need.

 

What part of this model is then the function of "endogenous retrovirus"?

 

Where is the paradigm shift?