Journal of Virology on XMRV, AZT, tenofovir, and raltegravir


Senior Member
NYC (& RI)
Abstract of the new paper:
In summary, the establishment of XMRV infection in patients may be dependent on infection of A3G/A3F-deficient cells and that cells expressing low levels of A3G/A3F, such as prostate cancer cells, may be ideal producers of infectious XMRV. Furthermore, anti-HIV-1 drugs AZT, tenofovir, and raltegravir may be useful for treatment of XMRV infection.
HIV-1 integrase inhibitor, raltegravir, was able to inhibit XMRV at nanomolar concentrations (0.82 0.07 nM), with XMRV being 2.5-fold more susceptible in comparison to HIV-1 (2.25 0.21 nM).

This makes me so happy!

Tina- AZT is so toxic it probably wouldn't be great for us since we are already so sensitive to meds and other 'insults' to our bodies.


Senior Member
How do the safety of tenofovir and raltegravir compare? Since it seems they needed at least twice as much tenofovir but only less than half as much raltegravir to inhibit XMRV compared to HIV.

Here's a gov't website about HIV drugs. I haven't read it yet.

Side effects are more of a concern for me than how much of each drug we need to take (i.e. potency). You might need twice drug A than B to defeat XMRV for example but if drug A is relatively safe and B has a lot of side effect, I'd still go with A.


Senior Member
This paper contains two different discussions. The second half is the drug testing that many have commented on but the first is about inbuilt defense mechanism in some cells. I am no expert at all but I wrote a little summary that I hoped would start a conversation about the first half of the paper too but it seems to have been buried under posts about the drug testing.

I hope this is a link to my simplistic view of a few things that jumped out at me from the paper - I don't seem to be able to get a link to just that post.

I would appreciate someone who understands some of this commenting on it too because it may be important in understanding which tissues or cells that XMRV can be easily found in and which will be much harder to find XMRV in. Is it why blood testing is so hard?


Well, I've tried to read through the full paper and although I've had to skim the most technical parts there are a few things that jumped out at me that I wondered if other people had noticed. I am in no way an expert in this and I may have got this completely wrong and I hope someone more knowledgeable may explain this better.

They examined how susceptible XMRV was to two build in defence mechanisms in the body - A3G and A3F. They found that it did affect the replication of XMRV and so XMRV grew better in cells without those mechanisms like LNCaP (prostate cancer cell line?) - the cell line that has been found to be best to grow XMRV. Could that be the reason why this cell line is so good an environment for replicating XMRV?

Also they found that the some cells like T cells and B cells do use this defense mechanism and can reduce the replication of XMRV. I got a little confused in this section because there was discussion of many different cell types that I'm not familiar with. In the conclusions though it say that some XMRV may still remain in these cells at a low level. Could this be why XMRV is harder to find in the blood?

They discovered that one of the ways the A3G and A3F reduce the replication is introducing mutations into the XMRV and they could see these mutations where the XMRV had been in contact with A3G and A3F.

Could these mutations that are introduced affect the type of testing where you look for specific sequences? I don't know if that is possible or if they affect the relevant part of the sequence.

From the conclusions

They also tested a variety of HIV drugs and found

Was a very technical paper and it was difficult to even understand the conclusions properly without a background in this area.

Hope that my inexpert comments may help to start a discussion.

APOBEC proteins are indeed a family

XMRV is a MuLV class gammaretrovirus.MuLV is sensitive to APOBEC 3B And 3G but NOT to other APOBEC proteins of any kind.So just because XMRV is sensitive to some it does not mean sensitive to all.

To effect replication these proteins must be incoporated into the new virus and bind with the RNA

The protein then deletes sections of the RNA so that the new virus can no longer replicate

The APO B and G types can bind and get incorporated

The MuLV gag sequence has evolved to prevent the binding of other APOTEC proteins allowing it to replicate(albeit at a reduced rate) in an otherwise toxic cellular environment.

If MuLV can do it it is likely that the greater number of deletions within the XMRV gag region will make it more efficient on blocking APO binding