why do symptoms vary with time an explanation -transposition of retroviruses(XMRV)

[Gerwyn]

A number of people with ME report that they have different symptoms at different times during their illness. This is difficult to explain with any other hypothesis apart from the involvement of XMRV.

XMRV could act as a gene hopper siliding about within the chromosomes of the same cell or different cells.

Gammaretroviruses prefer to integrate within the start sequences of genes.

So it is possible that they act as"puppet masters" for different abnormalities at different times leading to a particular pattern of symptoms at different times

Here comes the science bit:

Transposons are sequences of DNA that can move around to different positions within the genome of a single cell, a process called transposition.

In the process, they can cause mutations and change the amount of DNA in the genome.

Transposons were also once called jumping genes, and are examples of mobile genetic elements.

There are a variety of mobile genetic elements, and they can be grouped based on their mechanism of transposition.

Class II mobile genetic elements, or retrotransposons, copy themselves by first being transcribed to RNA, then reverse transcribed back to DNA by reverse transcriptase, and then being inserted at another position in the genome.

transposons were also once called jumping genes,or"Junk DNA"

Retrotransposons work by copying themselves and pasting copies back into the genome in multiple places.

Initially retrotransposons copy themselves to RNA (transcription) but, in addition to being transcribed, the RNA is copied into DNA by a reverse transcriptase (often coded by the transposon itself) and inserted back into the genome.

Retrotransposons behave very similarly to retroviruses, such as HIV.


There are three main classes of retrotransposons:

Viral: encode reverse transcriptase (to reverse transcribe RNA into DNA), have long terminal repeats (LTRs), similar to retroviruses

It is only comparatively recently that retroviruses have been recognized as particularly specialized forms of eukaryotic transposons.

In effect they are transposons which move via RNA intermediates that usually can leave the host cells and infect other cells. Or reintegrate in a different position in the DNA of the same cell

The extra chromosomal linear DNA is the direct precursor of the integrated element and the insertion mechanism bears a strong similarity to "cut and paste" transposition.

 

[oerganix]

A number of people with ME report that they have different symptoms at different times during their illness. This is difficult to explain with any other hypothesis apart from the involvement of XMRV.

XMRV could act as a gene hopper siliding about within the chromosomes of the same cell or different cells.

Gammaretroviruses prefer to integrate within the start sequences of genes.

So it is possible that they act as"puppet masters" for different abnormalities at different times leading to a particular pattern of symptoms at different times

Here comes the science bit:

Transposons are sequences of DNA that can move around to different positions within the genome of a single cell, a process called transposition.

In the process, they can cause mutations and change the amount of DNA in the genome.

Transposons were also once called jumping genes, and are examples of mobile genetic elements.

There are a variety of mobile genetic elements, and they can be grouped based on their mechanism of transposition.

Class II mobile genetic elements, or retrotransposons, copy themselves by first being transcribed to RNA, then reverse transcribed back to DNA by reverse transcriptase, and then being inserted at another position in the genome.

transposons were also once called jumping genes,or"Junk DNA"

Retrotransposons work by copying themselves and pasting copies back into the genome in multiple places.

Initially retrotransposons copy themselves to RNA (transcription) but, in addition to being transcribed, the RNA is copied into DNA by a reverse transcriptase (often coded by the transposon itself) and inserted back into the genome.

Retrotransposons behave very similarly to retroviruses, such as HIV.


There are three main classes of retrotransposons:

Viral: encode reverse transcriptase (to reverse transcribe RNA into DNA), have long terminal repeats (LTRs), similar to retroviruses

It is only comparatively recently that retroviruses have been recognized as particularly specialized forms of eukaryotic transposons.

In effect they are transposons which move via RNA intermediates that usually can leave the host cells and infect other cells. Or reintegrate in a different position in the DNA of the same cell

The extra chromosomal linear DNA is the direct precursor of the integrated element and the insertion mechanism bears a strong similarity to "cut and paste" transposition.

So, doing this in different cells, in different parts of the body, would result in these differing symptoms at different times? Is that what you are saying here?

(This post was picked up by my Google Alert for XMRV.)

 

[leelaplay]

I inferred the same as oeganix.

Hmmm - Gerwyn for the Nobel?

 

[Gerwyn]

So, doing this in different cells, in different parts of the body, would result in these differing symptoms at different times? Is that what you are saying here?

yes

 

[Rosemary]

'Copy-And-Paste DNA' More Common Than Previously Thought

..Source: University of Leicester
Tuesday, June 29, 2010

Finding has new implications for understanding genetic diseases

.Researchers at the University of Leicester have demonstrated that movable sequences of DNA, which give rise to genetic variability and sometimes cause specific diseases, are far more common than previously thought.

In a paper published in the leading journal Cell, Dr Richard Badge and his collaborators examined L1 (or LINE-1) retrotransposons: DNA sequences which can 'copy and paste' their genetic code around the genome. By breaking up genes, L1s can be responsible for some rare instances of genetic disease.

Working in collaboration with colleagues from the Universities of Michigan and Washington and the HHMI, the researchers developed an innovative technique to find L1s, using short sequences of DNA called fosmids. These are free-floating loops of DNA, which can be easily transported into bacterial cells, and can carry pieces of human DNA.

Each fosmid can hold only a specific amount of DNA, approximately 40,000 bases. So by comparing the two ends of a piece of human DNA held in a fosmid, against their known positions in the human genome sequence*, the scientists were able to quickly and easily spot differences in size.

"We're just looking at each end of the sequence and seeing if they're the right distance apart."explains Dr Badge. "This shows us the existence of insertions (which we're interested in) and also deletions. This technology is completely unbiased – it doesn't care what the insertion/deletion actually is, just whether it's there."

Having identified the insertions, the next step was to see if they could 'jump' in cultured human cells and how common they are – which is where the research team found something completely unexpected.

"Previous studies suggested that lots of L1s should jump - but don't," says Dr Badge. "But about half of the L1s we found jump really well, which was very surprising. We found about 65 elements, which had not been previously identified.

"This tells us that active human retrotransposons are much more common than we expected. Individual active L1 retrotransposons are quite rare - but there are a lot of them."

The paper 'LINE-1 Retrotransposition Activity in Human Genomes' by Beck et al is one of three L1 studies published in the 25 June 2010 issue of Cell. A commentary in the journal describes the team's results – 37 of the 68 elements studied being very active or 'hot' – as "incredible."

Because of the mistaken belief in their rarity, active retrotransposons have not been as closely studied as other sources of genetic variation, but this study and the others in the journal signify a developing acceptance of their significance.

"In this field, we are constantly fighting the perception that these bits of DNA are 'junk'," observes Dr Badge. "Actually they're very active and some of them have disease relevance. They are big bits of DNA so when they jump into a gene they disrupt the gene sequence and this can cause genetic disease

 

[BEG]

Rosemary,

Would you be so kind as to put your post into a paragraph using laymen's terms? I'm sure all of us here with cognitive difficulties would appreciate it. Thank you.

 

[determined]

I've wondered about the mechanism for this many times over the years. But Gerwyn, wouldn't the virus have to have some kind of concerted mechanism to affect enough cells in the exact same place, to cause symptoms at the level of the organism?