Interesting Articles on Mouse version of XMRV


Senior Member
Victoria, BC
Here are a couple more interesting articles showing how the mouse version of XMRV works...
Again, take my summaries with a grain of salt. I could have some aspect of the science wrong

B Lymphocyte Activation by Coinfection Prevents Immune Control of Friend Virus Infection1 -

In this one they found that even if a mouse would normally have the genetic ability to resist the virus if they first caught a different virus (LDV) they wouldn't be able to stop the retro-virus from infecting them. In humans this could explain the disease clusters. If some other virus acted as a helper for XMRV (One of the various ones people thought was the root cause over tha last 20 years) it could have an outbreak in an area followed by those who were infected by XMRV getting CFS.

Immune Control and Prevention of Chronic Friend Retrovirus Infection

This one describes the battle between the immune system and the related mouse retro-virus. How the virus escapes sounds similar to XMRV.

Race between Retroviral Spread and CD4+ T-Cell Response Determines the Outcome of Acute Friend Virus Infection

This article kind of summaries the top two. Interestingly, it seems like the immune system dysfunction described seems to mirror what happens in people with CFS.

Here is an interesting summary from that article "As with other retroviruses, FV establishes persistence and causes disease in virus-naive mice, in spite of the induction of a virus-specific primary immune response, and this ability of FV is amplified by additional genetic susceptibility or by coinfection."

It would be intersting for someone to contact 23andMe and see if we could use their system over time to find the genetic variation in something like MET that is causing the susceptibility to XMRV.


Senior Member
Interesting articles. Here is what the abstracts made me think of:

1. B-cell activation: interesting because EBV mono has been linked to development of CFS and EBV in particular causes B-cell to activate and produce a host of antibodies against EBV and other things. In fact, one of the EBV mono diagnostic tests uses production of these antibodies to indirectly test
for EBV infection. (heterophile antibodies)

2. CD4 and retroviral infections: This is similar to what happens in HIV infection where acute HIV infection induces a brief, mild flu-like infection in some people initially that only lasts a few days. They're fine after that for months to years, not developing opportunistic infections, until HIV starts to overwhelm CD4 and immune response leading to decreased CD4 count and the start of infections. It might be that the difference between acute vs. gradual onset CFS if CFS is caused by a retrovirus -- e.g. whether you go down with a crash or have gradual flu-like episodes leading to the crash depends on how each person's immune system reacts and what other bugs you encounter.

3. This also ties in with the work on HIV and quicker progression of HIV with particular co-infections.

4. Your last link goes to the same article?


Player in a Greek Tragedy
Matlock, Derbyshire, Uk
Tying up those loose ends

Thanks for finding these papers Impish.

You also summarised it well, Hope123 - Good work.

I like it when things tie up well with what we already know. There is surely value in that very fact, which others in positions of influence ought to be latching onto ?

TGOP :worried:


Senior Member
Say also, Hope, or anyone who knows, you mention b cell activation, I hadnt heard of that until recently, am trying to remember where I have just read about that in several places with cfs. Is it a marker or test like the nk cell? Could someone please give me quick summary/refresher on what the deal is with b cells and cfs?