I'm just going to explore a paper here that I think is interesting... It's a random paper that I found some time ago, and have just re-read it.
Please excuse me, because this is quite a rough and vague discussion about why this paper could be interesting, picking out vague connections that may or may not be significant...
Detection and immunochemical characterization of a primate type-C retrovirus-related p30 protein in normal human placentas.
Lois et al. 1984
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC391952/pdf/pnas00621-0247.pdf
"
We now report that normal human term placentas contain
a protein antigen of -30,000 daltons (under dissociating/
reducing conditions) that is physicochemically similar to
reference murine and primate type C retrovirus p30s and
antigenically cross-reactive with p30 of the SSAV/GaLV
primate retrovirus group."
12 out of 14 Normal Human Placentas were found to "
contain a protein or polypetide [...] that is antigenically cross-reactive with p30 core protein of the simian sarcoma-associated virus/gibbon ape leukemia virus [GALV] primate retrovirus group and is physicochemically similar to reference murine and primate retrovirus p30s."
(Interestingly, GALV is supposed to be very similar to XMRV, and it is also what the CDC are said to have contaminated DeFreitus' samples with.)
Now where have we come across the p30 protein before? I think it was in relation to Judy Mikovits' slide-gate research. I'm not sure if I am right about that? I need to look it up to check the details.
"P30" seems to be a very similiar, but not identical, protein, in many different viruses (i'm not certain about that tho).
If all p30s are very similar, then that makes this research very interesting.
In this paper, they seem to be suggesting that this could be human endogenous gene expression, rather than infection from an exogenous virus, or at least that is what they are interested in investigating:
"
This finding might lead to an understanding of endogenous type-C gene expression in humans."
I guess this study is a bit out of date because of the human genetic sequencing that has been carried out since 1984. They should know by now if humans carry endogenous type-c viral DNA.
But whether it is an endogenous or exogenous viral protein, it's interesting research...
Now why does the following sound familiar? Because JM found budding retroviruses revealed under electron microscope:
"
Electron microscope studies reveal the presence of budding type-C retrovirus like particles in virtually every normal human placenta examined."
It goes onto say that:
"
Recent investigations in molecular biology (13-16) indicate that normal human chromosomal DNA contains nucleotide sequences that are homologous to the genes of retroviruses previously isolated from mice and primates and have the structure of an integrated, but incomplete, type C retrovirus"
It's all food for thought.
The suggestion here is that the presence of the p30 protein could suggest that humans have type-c endogenous retroviruses, or partial retroviruses, that can be expressed in certain circumstances, such as in the placenta. These endogenous human retroviruses are similar to primate and
murine retroviruses.
It would be interesting to see how this info corresponds to more up-to-date info on the human genome, and whether the p30 protein can be expressed in human by endogenous retrorviral DNA.
How is all of this relevant?
1. If endogenous viral particles or proteins are being expressed within us, then I think that there is a possibility that they could interact with exogenous viruses if we are exposed to them, especially as the endogenous particles are so similar to murine viruses as this research suggests. I think Jamie Deckoff Jones says this type of event can happen.
2. If this paper detected exogenous viral particles, then it seems very similar to JM's research.
3. If the P30 protein is a consequence of endogenous viral gene expression, then this could be relevant to JM's work, in which she detected p30 proteins.
I think that the p30 protein is relevant to the work that Judy was doing (i'll have to look for her work again, to make sure i'm correct about that), and opens up the possibility that she was detecting the same p30 particles (either human endogenous or an exogenous infection).
This research paper led me to the following research paper which finds human endogenous retroviral sequences on the Y chromosome:
Human retroviral sequences on the Y chromosome
J Silver et al 1987
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC365247/
This got me thinking further... What if the X chromosome contains certain endogenous sequences that could interact with our immune system or with MLVs?
Would this make women twice as likely to get ill (if this was part of the mechanism of getting ME) because they have two X chromosomes? Or would their chances of getting ill be increased more than that, leading to a higher exposure to risk? i.e. twice the number of chromosomes could increase the risk of illness by four times.
What is the ratio of men to women with ME? I think it's said to be 4:1?
What if the risk of becomming ill is squared with each extra x-chromosome? So having two X-chromosomes means 4 times the risk of having one X chromosome. This would make the risk for women four times greater than for men. i.e. 4:1
My maths might be a bit dodgy there, but could this be a possible answer that would be worth investigating?
These are all very rough and ready thoughts, but i'd be grateful for any thoughts or feedback?