Antibodies to retroviruses in recent onset psychosis and multi-episode schizophrenia. (Not ME.)

[Bob]

This is an interesting study, and it answers some of the questions I've asked in the past about whether we have any MLV-like sequences in our genome. (Answer = we do.)

The study looks for MLV-like antibodies in patients with psychosis and schizophrenia. It finds increased levels of antibodies in patients with psychosis than in healthy controls, but did not find any in patients with schizophrenia.

They used assays to look for IgG antibodies to murine leukemia virus (MuLV), Mason-Pfizer monkey virus (MPMV), and feline immunodeficiency virus (FIV) by enzyme immunoassay utilizing whole virus and viral components.

But they do not seem to be concluding that there is an MLV infection, or other retrovirus infection, but they seem to be suggesting that there is an upregulation of MLV-like human endogenous retrovirus proteins.

I think this could potentially have implications for the antibodies found in ME patients.


Antibodies to retroviruses in recent onset psychosis and multi-episode schizophrenia.
Dickerson F, Lillehoj E, Stallings C, Wiley M, Origoni A, Vaughan C, Khushalani S, Sabunciyan S, Yolken R.
The Stanley Research Program at Sheppard Pratt, Baltimore, MD, USA.
Schizophrenia Research, 30 April 2012
http://www.ncbi.nlm.nih.gov/pubmed/22542615

"BACKGROUND:​

Immunological abnormalities involving the upregulation of endogenous retroviruses have been associated with schizophrenia in small studies."​

"RESULTS:
Compared with controls, individuals with recent onset of psychosis had increased levels of antibodies to MPMV and MuLV ... and increased antibody levels for defined portions of the MPMV and MuLV gag, pol and env proteins. The specificity of these antibodies was confirmed by Western blotting. Individuals with multi-episode schizophrenia did not show elevated antibody levels to any of the retroviruses measured. Infectious retroviruses were not detected in the blood of any participants."

This answered my question:

"Homology analyses indicated that there are multiple regions of the human genome homologous with MPMV and MuLV proteins, the highest being with the MuLV gag protein."

"CONCLUSIONS:
Antibodies to retroviral proteins are elevated in individuals with recent onset psychosis but not in individuals with multi-episode schizophrenia. The immunopathological consequences of this antibody response should be the subject of additional studies."

 

[GcMAF Australia]

there is a study stating that the human genome is "full of viral DNA sequences", it is unknown how many are functional.

 

[alex3619]

It is well established that our DNA is rich in inserted pathogen DNA, though nothing is ever proven in science. The presence of MLLV in our genome means we have been infected in the past. It makes it unlikely we are not currently infected - but this does not mean that infection is common, nor that it is particularly pathogenic. Our ancestors survived the original retroviral attack after all, in what were presumably harsh living conditions.

One of the things that inserted viral DNA might do is give us partial resistance. If they do become active from time to time - and it might be human DNA activating them deliberately - it would create targets for the immune system, a kind of self-immunization. It is when this goes wrong that we see problems. This in turn implies that some of these viruses were very dangerous, and hence drove evolutionary adaptation, which conflicts with the conclusion in the first paragraph.

Bye, Alex

 

[Bob]

Ah, yes, I got confused in my original post.
I had been wondering if our genome contains any XMRV-like sequences.
And, specifically, if we have XMRV-like sequences in any of our human endogenous retroviruses.
That question is still not answered for me by this study. Not in the abstract anyway.

I was thinking about the positive serology research that Mikovits and Hanson have carried out, and the possible origins of the antibodies. I was interested in whether there is a possibility that they are autoimmune antibodies, related to up-regulated XMRV-like human endogenous retrovirus genes.

Whatever the outcome of Lipkin's study, previous serology results have been more consistent than PCR results. I'm not sure about the blood working group study though. Someone told me that the serology results were unconvincing in the BWG study, and I haven't revisited it to check that out (memory useless.)

We have many human endogenous retroviruses, and I don't know the details of how many are MLV-like.
Studies into schizophrenia often look at upregulation of human endogenous retrovirus genes, with the potential for expressing human endogenous retrovirus proteins or partial proteins.

One theory about XMRV is that it could potentially interact or recombine with human endogenous retrovirus particles, in all people, or a just subset of the population, potentially creating new pathogens or new ways that an MLV-like virus might interact with our immune system. Another theory is that preXMRV mouse viruses might have interacted with human endogenous retrovirus particles, which then created XMRV in humans.

It's all food for thought.

 

[Dufresne]

Our ancestors survived the original retroviral attack after all, in what were presumably harsh living conditions.

Then again maybe a good number of them developed serious disease, and the weakest were filtered out. And I presume their harsh living conditions included a natural diet, lots of exercise, and a total lack of man-made chemicals and EMF.

 

[Mula]

There are around eight endogenous MLVs present in the human genome but the report above did not provide data to link the immune response they produced with their assay to any of those. That these may be expressing doesn't establish this relationship either because any infection is able to do this. The antibody response which has been previously detected uses an antibody which cannot bind to any of these endogenous viruses. Hypothetically the paper may have located a specific group of people who do have an infecting retrovirus but their assays were unable to locate said virus.