In the past there have been several viral candidates proposed as causative agents of ME/cfs
Any causative agent must be able to account for all the observed bioabnormalities in ME patients reported in studies involving correctly diagnosed patients.
In particular if a viral ageant is proposed as the causative ageant the properies of that virus must be able to account for
! post exertional malaise induced by physical or cognitive effort
2The abnormal expression of a large number of genes
The viral ageants so far do not exhibit the properties that can account for those observations and neither do Hervs..
The following attracted my attention
Infectious XMRV tends to insert into the human genome at
transcription start sites, CpG islands, DNase-hypersensitive
sites, and gene-dense regions [18].
XMRV inserts into the start "switches" of genes
XMRV was originally discovered in the start sequence of a CREB gene.
CREB/CRE proteins are involved in gene regulation in all bodily systems
Hence there is apossible mechanism whereby XMRV gan interfere with gene regulatory functions
But there are a wide range of abnormally regulated genes reported.
Rertoviruses are unique in being able to act as transposons in short they can move about the same chromosomes or different chromosomes in the same cells and or different cells
Hence XMRV has the potential to be a moblie gene regulator effecting the regulation of different genes at the same time or different times
Gammaretroviruses in general and MuLV in particular have been shown to to indirectly(Via NO production) and directly(via integration)damage mitochondria.Damage to Mitochondria (even if slight) would produce PEM.
No other class of virus has been shown to produce mitochondrial damage in this manner
Nitric oxide concentrations are elevated by the activation of IFN alpha.INFalpha is upregulated by CREB cre systems.XMRV integrates into CREB genes
Xmrv as a causative agent explains the observations in a way that no other class of virus can
The other parts of the paper that drew my attention was the following
XMRV is xenotropic because highly similar viruses exist in
the germline of mice, but their envelope (env) proteins no
longer have a receptor on murine cells [14••]. Although it
cannot reproduce in mice, the virus can bind to receptors in
other foreign (Greek xenos) species, including humans
and
It is not known when XMRV began to
infect humans, but it may have been within the last few
hundreds of generations given the 99% identity between the
six genomes that have been sequenced to date from
activated CFS leukocytes and advance
d prostate cancers
finally
XMRV proteins, RNA, and DNA were detected in plasma,
phytohemagglutin (PHA), plus interleukin-2–activated leukocytes
from CFS patients [2••, 3].
DNA sequencing
identified 736 nucleotides from XMRV Gag and 352 from
Env genes.
Now this author found the information from the science paper easily. I must ask why Mclure and Groom found it so difficult.
I must also ask why two renowned retrovirologists looking for a RNA virus did not look for viral RNA
I read the excellent article with Proff Goff.Bearing in mind that there are at least six strains of XMRV one of his sentences hit me like a club between the eyes.
He said that you only have to get your pcr primer wrong by only two neuclotides and you would not find the virus you were looking for if it was a different strain.
McClure and Groom would never have found different strain because their primer was based on a partial V62 clone