Six strains of XMRV so far!

[citybug]

Is there a study part in this (no access yet) or is it an article, spreading the word to doctors? So many people, even patients say another virus, they don't want to hear about it.
Could neurotoxic envelope proteins on the XMRV be related to the proteins that Baraniuk is finding in spinal fluid?
I'm at the page in Osler's web where viruses are budding all over the CDC lab from contamination, possibly from a patient's spinal fluid. Maybe de Frietas's virus was the epidemic one, and XMRV in the CFS patients from Atlanta. Sorry about the speculation, I'm thinking class action suit.

One theory about HIV or ebola is that encroaching on the forests brought us closer to the monkeys.

 

[justinreilly]

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.

What about CAV (DeFreitas retrovirus)? In her patent app there was an electronmicrograph of CAV inside an abnormally distended mitochondrion. According to Osler's Web, no other virus has ever been found inside an animal's (including humans') mitochondria. I, as a layperson, think it's probable that CAV and XMRV work in concert to cause ME. I have no idea about CAV's effect on genes. I'd be fascinated to hear your take Gerwyn (and others).

 

[justinreilly]

I'm at the page in Osler's web where viruses are budding all over the CDC lab from contamination, possibly from a patient's spinal fluid. Maybe de Frietas's virus was the epidemic one, and XMRV in the CFS patients from Atlanta.

CDC later claimed the contaminant was a gibbon leukemia virus.

 

[_Kim_]

CDC later claimed the contaminant was a gibbon leukemia virus.

How did Dr. Yes get into De Freitas' Lab?

 

[Dr. Yes]

HEY...WHAT WAS THE CDC DOING WITH GIBBONS ??

:Retro mad::Retro mad:


I have..v-vague memories.. so unclear.. cold laboratory... white lab coats... anal probes..
...no, surely, it must all have been a dream, a TERRIBLE DREAM...
​

 

[citybug]

I Even the NIH has said, after pretty blankly stating at one point that they're not interested in pathogens, that they do have some interest in pathogens in CFS now. They did (finally) fund the WPI's big immune study.

Do you mean the study with Kerr that got cancelled? So far WPI has been saying they haven't been funded in general. Are there new funds?
I think there is no thread for the HHS study, and WPI is doing all these things with the feds but with their own money.

(not in WSJ, on CAA page) The HHS Blood XMRV Scientific Research Working Group with DHHS Office of Public Health and Science, NIH, CDC, FDA and Suzanne Vernon has a study on Cort's Study page. They have stage 1) validate laboratory methods and reagents for XMRV testing., test 1,200 healthy donors’ blood samples and 100 CFS patients’ samples collected by Dr. Judy Mikovits, stage 2) assess the prevalence of XMRV in the general population and blood supply, as well as in other CFS patient cohorts, stage 3) studies to understand how XMRV is transmitted, whether it causes human disease, and how it affects various subgroups of the population.


Different group from the study in Wall St. Journal coordinated by the XMRV Working Group (from conference?) They'll be comparing their results of 6 labs on testing samples, to see if they have an accurate test. The second phase is looking at 350 samples of different types, and later they would see if can be transmitted by blood donors. According to Amy Marcus of the WSJ, iIn the first phase, the labs include CDC, FDA with two different ones, NCI, Whittemore Peterson Institute’s lab, and Blood Systems Research Institute.

 

[natasa778]

don't remember if they (WPI) suggested PCR didn't work because of nucleotide variance with the primers used

They did mention that primers can account for negative results

 

[Gerwyn]

What about CAV (DeFreitas retrovirus)? In her patent app there was an electronmicrograph of CAV inside an abnormally distended mitochondrion. According to Osler's Web, no other virus has ever been found inside an animal's (including humans') mitochondria. I, as a layperson, think it's probable that CAV and XMRV work in concert to cause ME. I have no idea about CAV's effect on genes. I'd be fascinated to hear your take Gerwyn (and others).

Hi JustinReilly,

I know Mulv integrates into mitochondria CAV is a DNA virus unusually with a circular genome.

I believe it has been found within the rough endoplasmic reticulem of Mitochondria.It does not intigrate within the genome

.It slso cant act as a transposon.

Could it act in concert with XMRV yes I think it could as far as magnifing mito damage is concerned.

I am assuming we are talking about the CAV like virus the human circoviridiae.

it lacks an envelope and would probably not produce much of an initial immune response.

I didnt know that the defreitas virus was a CAV type.Thanks very much for telling me.I thought it was a retro.

A CAV infection could have been onvolved the outbreaks.Being naked DNA freezing could easily destroy any viable virus which would explain why the CDC could not find it in frozen samples.

The proteins it makes could have prion like properties.

I will look into the possiblity of the proteins having gene regulatory properties

cheers
Gerwyn.

 

[Gerwyn]

The word strain is being confused in this thread.

In the paper it says that the six different strains were the only isolates which have had their genome fully sequenced, and all showed 99% identity. This means that if every patient who was XMRV positive had their XMRV sequenced, then there would be as many different strains as there were XMRV positive patients. It's not talking about a different type or kind of XMRV, although in Walid Heneine/the CDC's presentation at the CROI, he did say that the CDC found a different variant of XMRV, and that this means that there is more divergence than previously reported.

I'm not sure what the correct term is, 'strain', 'type', or whatever, but the 'six strains' in the Baraniuk paper wasn't referring to what everyone is taking it to mean.

hi
so far 5 strains have been found in the total number of people who have that their XMRV sequenced.The different strains are almost identical but differe in their exact neucletide sequences.A good number of patients have the same strain others a different strain.that does not mean that they are different types or subgroups or produce different antibodies(although the latter is possible).The nucleotide sequences are not unique to an individual but are produced by slight changes in the reading frame of RT which does not have a stop codon.

 

[Summer]

WPI on CAV

I didnt know that the defreitas virus was a CAV type.Thanks very much for telling me.I thought it was a retro.



Gerwyn.

Gerwyn, I snipped out most of your post. Here is what WPI posted about CAV:

XMRV is Not the retrovirus identified by De Freitas et al.
the publication and patent submitted by De Freitas et all clear describe the molecular characteristics of a retrovirus that is not a gamma (type C) retrovirus. The patent submitted for the retroviruses states " "Chronic Fatigue Immunodeficiency Syndrome-associated virus, hereafter referred to bythe name CAV may be morphologically characterized as a retrovirus, particularly a non-C retrovirus which is capable of infecting humans. Electron microscopy of viral
particles formed in infected human cell cultures suggests that CAV is a non-C-type retrovirus because of its diameter, morphology, formation and location of intracellular virions. The Electon micrographs of XMRV shown in Lombardi et al clearly depict a budding type C retrovirus of 90-100microns The DeFritas patent goes on to say "More specifically, CAV-infected cells could be characterized by electron-dense circular virions, some with electron-luscent cores and
others with electron-dense cores, associated with the rough endoplasmic reticulum and inside large abnormally distended mitochondria in the cells. All particles are the same shape and size, 46-50 nm. No extracellular virus is observed. No forms budding from the cytoplasmic membranes are observed. Thus, CAV-infected cells could also be charcterized by the presence of intracytoplasmic particles"Gamma (type C) retroviruses are 90-1100uM as shown in Lombardi et al and all are shown to consist of electron dense cores and specifically to bud extra-cellularly not intracellularly.
The data describes in the Defreitas patent can be found at:http://www.ncf-net.org/forum/revelations.html These data are indisputable that XMRV is NOT the retrovirus described by De Freitas et al.

http://www.facebook.com/notes/whittemore-peterson-institute/fact8/184085913025

Gerwyn, I have the patent on her virus in PDF form. PM me if you would like me to email it to you.

Summer

 

[Adam]

How did Dr. Yes get into De Freitas' Lab?

Dr Yes on the left of picture?

I'm not an expert here, but I'd say either way, fake gibbon, faux gibbon or pseudo gibbon with false gibbon beliefs.

Is that blanket crocheted BTW? And is it me or does the REAL gibbon look a tad spaced out or has it just developed post anal probe gratification syndrome?

Really folks, when you add it all up, well...you have to say - it doesn't add up?

 

[starryeyes]

hi
So far 5 strains have been found in the total number of people who have that their XMRV sequenced. The different strains are almost identical but different in their exact neucleotide sequences. A good number of patients have the same strain others a different strain. That does not mean that they are different types or subgroups or produce different antibodies (although the latter is possible). The nucleotide sequences are not unique to an individual but are produced by slight changes in the reading frame of RT which does not have a stop codon.

I thought I'd try out the Editor Mode button on the right. I corrected your paragraph above Gerwyn and thought the corrections would show since I clicked that button. I was just curious. It looks like they don't show so I'm not really sure what it's for.

Anyway, thank you very much for posting this interesting article and for explaining it to us.

And it looks like you discovered the problems other researchers are having:

Gerwin wrote: 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

Great job Gerwyn!

 

[justinreilly]

Hi JustinReilly,

I know Mulv integrates into mitochondria CAV is a DNA virus unusually with a circular genome.

I believe it has been found within the rough endoplasmic reticulem of Mitochondria.It does not intigrate within the genome

.It slso cant act as a transposon.

Could it act in concert with XMRV yes I think it could as far as magnifing mito damage is concerned.

I am assuming we are talking about the CAV like virus the human circoviridiae.

it lacks an envelope and would probably not produce much of an initial immune response.

I didnt know that the defreitas virus was a CAV type.Thanks very much for telling me.I thought it was a retro.

A CAV infection could have been onvolved the outbreaks.Being naked DNA freezing could easily destroy any viable virus which would explain why the CDC could not find it in frozen samples.

The proteins it makes could have prion like properties.

I will look into the possiblity of the proteins having gene regulatory properties

cheers
Gerwyn.

Sorry to confuse you; no, actually 'CAV' meaning the name and acronym DeFreitas gave to her retrovirus on her patent app: Chronic Fatigue Syndrome Associated Virus (CAV). It is, as you noted, a retrovirus. And it most closely resembled Simian D Virus (with some sequences similar to HTLV 2).

 

[usedtobeperkytina]

Yes, whatever is causing CFS has to be VERY recent, very new, I don't think it passed "within the last 100 or so generations" or “less than 1000 years ago” as we would have seen CFS in humans sooner.

IMO only two versions are possible, either whatever is causing CFS has entered humans VERY recently, less than 100 years ago.

Or the causative agent/s have been around for longer but something new in the environment (toxins, pesticides etc) have caused IT to mutate and become pathogenic.

That is why I don’t buy the theory of “eating mice” causing xmrv to jump species – people have eaten mice throughout history, if nothing else then out of necessity throughout long periods of hunger and wars, and unfortunately there have been plenty of those in human history. Same with HIV – if it jumped from monkeys because of some odd tribal customs, or some naughty monkeys biting men, well those things would have been happening throughout history and still HIV waited to jump over until now.

Could it be that it has been in human population longer but goes into dormancy often. And it therefore doesn't transmit as much as HIV. And therefore only recently it has built up to the point that large numbers in population are getting sick.

Also, (and folks, don't jump on me for this) could it be that our stressful society creates a chronic cortisol high level that leads to more XMRV replication which means more people will see their immune system lose the fight.

Could birth control pills contribute?

Tina

 

[Snow Leopard]

Gerwyn now if you've worked it out lets hope others can, quickly.

Hypotheses are a dime a dozen, the real test is proving it.

 

[Gerwyn]

Hypotheses are a dime a dozen, the real test is proving it.

Hypotheses which purport to explain observations in ME patients are actually quite rare.Speculation in the other hand is rife.There is a big difference between the two.Hypotheses can be falsified speculation cant be because it is not based in obervations in vivo

 

[Gerwyn]

Sorry to confuse you; no, actually 'CAV' meaning the name and acronym DeFreitas gave to her retrovirus on her patent app: Chronic Fatigue Syndrome Associated Virus (CAV). It is, as you noted, a retrovirus. And it most closely resembled Simian D Virus (with some sequences similar to HTLV 2).

no worries.

For what it is worth i think that the Defreitas virus could have caused the outbreaks

Now, 30 years later after the initial discovery, 4 HTLVs are well established. HTLV-1 and HTLV-2 are both involved in actively spreading epidemics, affecting 15-20 million people worldwide.4 HTLV-1 is the more clinically significant of the two, as it has been proven to be the etiologic agent of multiple disorders. At least 500,000 of the individuals infected with HTLV-1 eventually develop an often rapidly fatal leukemia, while others will develop a debilitative myelopathy, and yet others will experience uveitis, infectious dermatitis, or another inflammatory disorder. HTLV-2 is associated with milder neurologic disorders and chronic pulmonary infections. The novel HTLV-3 and HTLV-4 have been isolated only in a few cases; no specific illnesses have yet been associated with these viruses.
Pathophysiology

HTLVs are intracellular proviruses that pass through formation of a "virological synapse", allowing the viral genome to be passed from one cell to another. Once infection has occurred, little replication takes place. Infection affects the expression of T-lymphocyte gene expression, leading to increased proliferation of affected T lymphocytes. HTLV primarily affects T lymphocytes: specifically, HTLV-1 predominantly affects CD4 lymphocytes, while HTLV-2 predominantly affects CD8 lymphocytes. In vitro, HTLV-1 is also capable of infecting other cell types, possibly accounting for the diverse pathogenesis of HTLV-1. Recently, GLUT-1, a ubiquitous glucose transporter, has been identified as a receptor for HTLV-15 ; this may explain its ability to infect various cell types.

note the mode of transfer cell to cell without having to enter the bloodstream.XMRV is thought to do the same

 

[natasa778]

note the mode of transfer cell to cell without having to enter the bloodstream.XMRV is thought to do the same

Could this possibly result in absence of virus-specific antibodies?? Would it be theoretically possible for such a sneaky virus to totally bypass the immune system in some cases, so no antibodies are created at all?

Asking 'cos of puzzling results that were presented by Abbotts guy at the CROI, where only a couple of people had antibodies to it, out of 800 or so tested.

 

[Gerwyn]

Could this possibly result in absence of virus-specific antibodies?? Would it be theoretically possible for such a sneaky virus to totally bypass the immune system in some cases, so no antibodies are created at all?

Asking 'cos of puzzling results that were presented by Abbotts guy at the CROI, where only a couple of people had antibodies to it, out of 800 or so tested.

in theory yes it could

 

[justinreilly]

no worries.

For what it is worth i think that the Defreitas virus could have caused the outbreaks

Now, 30 years later after the initial discovery, 4 HTLVs are well established. HTLV-1 and HTLV-2 are both involved in actively spreading epidemics, affecting 15-20 million people worldwide.4 HTLV-1 is the more clinically significant of the two, as it has been proven to be the etiologic agent of multiple disorders. At least 500,000 of the individuals infected with HTLV-1 eventually develop an often rapidly fatal leukemia, while others will develop a debilitative myelopathy, and yet others will experience uveitis, infectious dermatitis, or another inflammatory disorder. HTLV-2 is associated with milder neurologic disorders and chronic pulmonary infections. The novel HTLV-3 and HTLV-4 have been isolated only in a few cases; no specific illnesses have yet been associated with these viruses.
Pathophysiology

HTLVs are intracellular proviruses that pass through formation of a "virological synapse", allowing the viral genome to be passed from one cell to another. Once infection has occurred, little replication takes place. Infection affects the expression of T-lymphocyte gene expression, leading to increased proliferation of affected T lymphocytes. HTLV primarily affects T lymphocytes: specifically, HTLV-1 predominantly affects CD4 lymphocytes, while HTLV-2 predominantly affects CD8 lymphocytes. In vitro, HTLV-1 is also capable of infecting other cell types, possibly accounting for the diverse pathogenesis of HTLV-1. Recently, GLUT-1, a ubiquitous glucose transporter, has been identified as a receptor for HTLV-15 ; this may explain its ability to infect various cell types.

note the mode of transfer cell to cell without having to enter the bloodstream.XMRV is thought to do the same

Thanks for the info, Gerwyn. Is that really you? You can type!

That you think DeFreitas' rv could have caused the outbreaks is persuasive to me. Also, nice info on HTLVs.