Discussion in 'XMRV Testing, Treatment and Transmission' started by mojoey, Sep 5, 2010.
m0joey.....yea..just thought it might be newsworthy...
2 days on LDN and 2 days in bed...I knew it wasnt for me
Thanks Joey - I'm trying to drink from a firehose in this area.
ETA: In my case all in the spirit of There's No Such Thing As A Stupid Question, only Stupid People Asking Questions.
Any news about shifting more to therapies that focus on innate immunity, even for an infectious as noxious as HIV, is good news here. It gives us hope that we won't need to rely on ARVs forever, even if we need to start on them for a few years before these drugs go through IND and clinical trials.
No such thing as stupid here, period! It's been a trickle here, so bring on the hoes to dig in, the hose to drink from, the ho's to...
Well maybe not. As Michael Scott famously said, I aint yo ho, no mo.
there are these drugs - Miltefosine (Edelfosine) and Perifosine, which are being studied because they can kill HIV-infected macrophages.
Isn't it interesting that Edelfosine was also shown to be of use in chronic lymphocytic leukemia and mantle cell lymphoma?
I agree. If the monoclonal antibody works for prostate cancer, then that's a good indication.
I am not a expert on these things. It's a bit learn as we go. I did a search now for TSG101 and monoclonal antibodies. See here:
http://www.biocompare.com/ProductLi...ptibility-gene-101.html?types=6-74014&sb=true (scroll down on the screen)
It seems to me that it's pretty common that monoclonal antibodies work on the TSG101...
If that's the case, then I'd say it's good news.
Did you get a reply from the person posting about the TSG101 peptide? I'd really like to hear more about that.
Any idea why she says this? I can't read German!
I haven't read the entire article, but I don't think a reason is given. It's stated as a fact that large doses of AZT and Tenofovir are needed to inhibit XMRV. It's also stated that Raltegravir needs only small doses to inhibit XMRV. For this information they are pointing to other studies that have been done.
There's a catch mentioned in the article that we already knew: it looks like XMRV has a low replication rate and these antivirals are used to block replication... meaning they might not be really effective in treating XMRV.
The article concludes with a statement that XMRV might be the third retrovirus infecting humans and that both researchers and patients have a strong interest in XMRV. Then you get the usual questions/disclaimers: what percentage of people is infected? how is it transferred? does XMRV cause disease or is it a bystander? So the conclusion is that many questions are still unanswered.
I think it's good PR for the virus though. There can't be enough articles about it (unless the science is really bad).
why would it be high doses of tenofovir? i thought it was the same as the HIV dose
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