Not xmrv but herv k?!

[leaves]

Huber found herv k 18 in the blood of ME patients. This week a study found that herv k is the potential cause of the neuroimmune disease ALS
See http://www.sciencedaily.com/releases/2011/03/110302121911.htm
They say that herv k can activate after immune triggers and infections, and that it can be treated with herv sensitive ARV.

In my family I can trace back neuroimmune disease at least 100 years.
Altho I'm xmrv positive I think that Herv-k for me is a more likely explanation.
Thoughts?

 

[camas]

It would be wonderful if this pans out for ALS patients. I know someone who has lost two sisters -- one to CFS and the other to ALS which is a little unnerving. He's in the medical field, so I'll have to run these studies by him.

 

[Emmanuelle]

Okay, I'm a little freaked out ... my mother died of ALS. I've never heard of herv k! But I'm going to link to the site you posted and read about this right now. And ARV as well-- glad that there may be some treatment. (And I think my Mom had ME/CFS for years, but nobody knew about it then ... interesting.) Thanks for this info!

 

[leaves]

This is another interesting article that explains how herv can cause disease. It's about herv-w which is a potential cause for ms and schizophrenia
http://discovermagazine.com/2010/jun/03-the-insanity-virus

Note that HIV can also cause ALS and viruses as ebv are known to activate herv. It is possible that xmrv is a cofactor: eg xmrv+herv k 18= ME
Or maybe you don't need xmrv...

 

[undcvr]

It's still a retrovirus, we still dont have ARVs that work well against it.

 

[LJS]

The interesting thing about this finding is if they can identity the genes that cause ALS, in this case a possible ERV, it may yield some hope of treating it and other similar conditions. What I do not understand is this

Researchers might eventually be able to fight ALS, Nath adds, using antiretroviral drugs specific to HERV-K

Huh?? How can you treat a endogenous retrovirus (ERV) with antiretrovirals? This is my understanding of a ERV: it is not an active infection (does not and can not actively infect cells) and can not be transmitted from person to person. I thought you could just think of ERVs as part of someone's genes and not as a retrovirus because it basically is that at this point. It is part of the huge amount of garbage DNA all humans have left over from past retrovirus infections hundreds of thousands if not millions of years ago. So can someone clear up how you would be able to do anything with a antiretrovirals on a ERV?

 

[jace]

Hi LJS, your post sent me on a hunt round scientific papers. I found this the most illuminating

Human endogenous retroviruses (HERVs), probably representing footprints of ancient germ-cell retroviral infections, occupy about 1% of the human genome. HERVs can influence genome regulation through expression of retroviral genes, either via genomic rearrangements following HERV integrations or through the involvement of HERV LTRs in the regulation of gene expression. Some HERVs emerged in the genome over 30 MYr ago, while others have appeared rather recently, at about the time of hominid and ape lineages divergence. HERVs might have conferred antiviral resistance on early human ancestors, thus helping them to survive. Furthermore, newly integrated HERVs could have changed the pattern of gene expression and therefore played a significant role in the evolution and divergence of Hominoidea superfamily. Comparative analysis of HERVs, HERV LTRs, neighboring genes, and their regulatory interplay in the human and ape genomes will help us to understand the possible impact of HERVs on evolution and genome regulation in the primates. BioEssays 22:161171, 2000. 2000 John Wiley & Sons, Inc.

So it seems that though they are only passed on through the DNA from parent to child, they do express their genes, which means presumably that they increase their population in the host.

Still doesn't answer if anti-retrovirals will control that expression I highlighted - perhaps reverse transcriptase inhibitors would though (I'm guessing here) if the HERV's are expressing gene fragments, as they might stop these new HERV babies from finding a cosy bed in the host cells...

Some people think that these here retroviruses are a driver of evolution, and what triggered some of the apes to transform over time into hominids.

 

[redo]

Nice find leaves. Thanks for posting.

 

[redo]

Huber found herv k 18 in the blood of ME patients. This week a study found that herv k is the potential cause of the neuroimmune disease ALS
See http://www.sciencedaily.com/releases/2011/03/110302121911.htm
They say that herv k can activate after immune triggers and infections, and that it can be treated with herv sensitive ARV.

In my family I can trace back neuroimmune disease at least 100 years.
Altho I'm xmrv positive I think that Herv-k for me is a more likely explanation.
Thoughts?

I think we're harboring a virus (which many, many people have latent) which may in many cases be transferred from mother to child, and thereby go in generations (it may be XMRV, it may not).

The virus may activate when we are exposed to pressure to the immune system (vaccines, influenza, EBV, severe stress etc), and thereby break out. The virus will act synergistically with some infections, and can cause different expressions (such as CFS, MS, ALS, Fibromyalgia etc).

That's what I think.

 

[justy]

Thanks Leaves, found this on Hubers labsite which states " Activation of HERV-K18. The HERV-K18, an endogenous human retrovirus can be activated in the course of several types of responses and affect the outcome of EBV infection and influence autoimmune disease."

So whilst it is an endogenous retrovirus it can be activated and influence disease progression- have i got that right? Interesting that they mention EBV infection.
Do you have a link to show her work which found it in the blood of M.E patients. Also what does this mean if it is found in the blood, surely if its an endogenous retrovirus then we would all have it in us. Sorry if thats very simplisitc thinking -im a simple girl! can anyone explain?

 

[ukxmrv]

Huber spoke at last years UK Invest in ME conference for anyone interested. If you order the DVD from their website you can see/hear the talk.

I think from memory that were some posts last year (?) to this forum from people involved in the Huber study. If you search you should find the earlier threads on this topic.

It's not XMRV related so maybe should be moved or added to the previous threads? Although Huber spoke about her attempts to find XMRV at the Invest in ME conference as well.

 

[leaves]

I think this is very much related to xmrv, as it is also a retro virus and as xmrv and herv may have an interaction that causes the disease (as hiv and herv-k do cause ALS)

 

[redo]

Perhaps a bit offtopic, but interesting to see that it's being tried artemisinin for HERV-W

She is running a clinical trial to examine whether adding an anti-infective agent called artemisinin to the drugs that patients are already taking can lessen the symptoms of schizophrenia. The drug would hit HERV-W indirectly by tamping down the infections that awaken it. “If we can treat the toxoplasmosis,” Torrey says, “presumably we can get a better outcome than by treating [neurotransmitter] abnormalities that have occurred 14 steps down the line, which is what we’re doing now.”

http://discovermagazine.com/2010/jun/03-the-insanity-virus/article_view?b_start:int=3&-C=

 

[Grape Funk]

Check this out:

EBV LMP-2A employs a novel mechanism to transactivate the HERV-K18 superantigen through its ITAM.

Hsiao FC, Tai AK, Deglon A, Sutkowski N, Longnecker R, Huber BT.

Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA.
Abstract
EBV encodes latent membrane protein (LMP)-2A that functions as a homologue of the activated BCR. We have previously shown that LMP-2A transactivates a human endogenous retrovirus, HERV-K18, in infected B-lymphocytes. The Env protein of HERV-K18 encodes a superantigen that strongly stimulates a large number of T cells. To delineate the mechanism through which LMP-2A transactivates HERV-K18 env, we tested a panel of tyrosine mutants of LMP-2A in a murine B lymphoma that stably harbors HERV-K18. Our analysis revealed that the immunoreceptor tyrosine-based activation motif (ITAM) of LMP-2A is important for HERV-K18 env transactivation. ITAM contains 2 tyrosines that initiate signaling cascades when both residues are phosphorylated. However, in our study, single-tyrosine mutants of ITAM still retained full induction of HERV-K18 env. After truncating 25 kb of genomic sequence downstream of HERV-K18, LMP-2A failed to transactivate HERV-K18 env. Thus, an LMP-2A-inducible element is located downstream of HERV-K18.

 

[redo]

Great find GF!

I searched for other studies from the same authors, and found this:

Here we show that the human lymphotropic herpesvirus Epstein-Barr virus (EBV) transcriptionally activates the env gene of an endogenous retrovirus, HERV-K18, that possesses SAg activity.

http://www.ncbi.nlm.nih.gov/pubmed/11672540

 

[TheMoonIsBlue]

I remember someone on ProHealth posting they had taken part in study on HERV and ME/CFS-that was quite a while back. I think I remember it was a study at some fairly major research hosptial. I have no idea what became of the study. Does anyone know?

And NO effective treatment for HERV?

 

[Grape Funk]

I was reading the article provided - http://discovermagazine.com/2010/jun/03-the-insanity-virus/article_view?b_start:int=1&-C= ..... And i found some massively interesting facts on the schizophrenics illuminated throughout the journalism that pertained to myself in some ways. For one, i got EBV four years ago, mono 6 months later, then cfs. I'm born April 2nd (supposed to pop out in first week march). I was 19 when i first contracted EBV. No more brain fog for me, but feels like my head is inflamed and filled with water like fluid sometimes ( I don't know if anyone has ever felt that as a symptom of CFIDS before). Here's the craziest part spoken by Dr. Torrey (his sister had schizophrenia) :

“If you look at the blood of people with schizophrenia,” Torrey says, “there are too many odd-looking lymphocytes, the kind that you find in mononucleosis.” And when he performed CAT scans on pairs of identical twins with and without the disease—including Steven and David Elmore—he saw that schizophrenics’ brains had less tissue and larger fluid-filled ventricles.
Subsequent studies confirmed those oddities. Many schizophrenics show chronic inflammation and lose brain tissue over time, and these changes correlate with the severity of their symptoms. These things “convinced me that this is a brain disease,” Torrey says, “not a psychological problem.”

Add to this 15 to 25 is regarded as span for onset, and schizophrenics born in winter to early spring months, its suspicious to say the least. The HERV k18 is lookin good. But, it may all be coincidental, God knows.

On another note, i will disperse this knowledge. Superantigens can be a result of HERV k18, and these proteins can activate certain immune T cells and cause autoimmunity. Once, again, i have not been "sick" beside my normal chronic sinusitis and PEM when i over exert my limits (the usual flu like sh!t prevails). Maybe someone can relate, i'm just thinking out loud. I know possibilities are infinite and answers are a shooting star.

 

[Grape Funk]

Another One For The Record

Epstein-Barr virus transactivates the human endogenous retrovirus HERV-K18 that encodes a superantigen.

Sutkowski N, Conrad B, Thorley-Lawson DA, Huber BT.

Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA.
Comment in:

Immunity. 2001 Oct;15(4):503-6.
Abstract
Superantigens (SAgs) are proteins produced by pathogenic microbes to elicit potent, antigen-independent T cell responses that are believed to enhance the microbes' pathogenicity. Here we show that the human lymphotropic herpesvirus Epstein-Barr virus (EBV) transcriptionally activates the env gene of an endogenous retrovirus, HERV-K18, that possesses SAg activity. SAg activity was demonstrated by MHC class II dependent preferential activation of TCRVB13 T cells in response to murine B cells transfected with the HERV-K18 env gene. This is a unique demonstration of a pathogen inducing a host-encoded Sag and accounts for the previously described EBV associated Sag activity. The T cell activation elicited by the Sag could play a central role in EBV infection and associated diseases.

 

[redo]

In one experiment, Perron isolated HERV-W virus from people with MS and injected it into mice. The mice became clumsy, then paralyzed, then died of brain hemorrhages. But if Perron depleted the mice of immune cells known as T cells, the animals survived their encounter with HERV-W. It was an extreme experiment, but to Perron it made an important point. Whether people develop MS or schizophrenia may depend on how their immune system responds to HERV-W, he says.

www.discovermagazine.com/2010/jun/03-the-insanity-virus/article_view?b_start:int=2&-C=

I think this is an important point... It may be that some people get different immune responses (from XMRV, HERV or others) and they get CFS, MS, mental problems or perhaps even RA.

How the immune system reacts seems to be important.

 

[redo]

I am bumping this thread. It's a good read for those who haven't browsed through it yet.