As a newbie to retroviruses, I wanted to learn a bit more about antiretroviral therapy. What is it? What are the different classes of drugs that are being discussed? How does it work in HIV, and how might this be different in XMRV? So... if you liked the video animation of XMRV on the Dr. Oz show ( http://www.youtube.com/watch?v=_WEUC7hRXzM ), here's "Version 2.0" from a science museum, with quite interesting details of how the key classes of antiretroviral drugs work: How do Antiretroviral Drugs Work video from the Koshland Science Museum Website: http://www.koshland-science-museum.org/exhib_infectious/hiv_antivirals_movie1.jsp I've watched it once, and it was quite a work-out , but things did make more sense by the end of the short video. I think I'll have to watch it a few times to "get it", and even then - because of XMRV's purported slow transcription rate - all of these classes of antiretrovirals may not be completely relevant. Or would they?? Here are some more interesting tidbits on antiretroviral drugs: (I recommend you watch the linked video above first, then look at the descriptions below) From: http://www.apositivelife.com/forasos/slowing-down-hiv.html HIV treatment: slowing down HIV Antiretroviral drugs work by keeping HIV from multiplying. There are five kinds of antiretroviral drugs approved by the US Food and Drug Administration, which attack four different phases of the HIV reproductive cycle (Department of Health and Human Services [DHHS], 2005). Current antiretroviral HIV medications fall into five classes: Entry inhibitors Nucleoside reverse transcriptase inhibitors (NRTIs) Non-nucleoside reverse transcriptase inhibitors (NNRTIs) Integrase inhibitors Protease inhibitors Here is how each class of HIV antiretroviral drug works: Entry Inhibitors: To make copies of itself, HIV first uses its spikes to fuse with the host cells membrane, and then thrusts its contents inside. Coreceptor blockers keep HIV from locating the host cell membrane. Fusion inhibitors work by attaching themselves to one of the proteins on HIV's spikes, which makes the HIV spike unable to fuse with the host cell Nucleoside Reverse Transcriptase Inhibitors (NRTIs): To make copies of itself, HIV uses an enzyme called reverse transcriptase to convert its RNA into DNA after the virus enters the host cell. NRTIs are faulty versions of molecules used to build a DNA chain. When the HIV attempts to turn its RNA into DNA, NRTIs cause the DNA chain to be incomplete, resulting in DNA that cannot create new copies of the virus Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): Like NRTIs, NNRTIs also interfere with reverse transcriptase. NNRTIs chemically bind to reverse transcriptase and make it unable to do its job Integrase Inhibitors: Once the new DNA chain is finished, it enters the host cell's nucleus and splices itself into the host cells DNA using an enzyme called integrase. Integrase inhibitors chemically bind to integrase and stop it from working, so the virus's DNA is never incorporated into the host cell's DNA Protease Inhibitors (PIs): After HIV hijacks a cell's nucleus to make copies of itself, it needs an enzyme called protease to chop its long chains of proteins into infectious bits. Protease inhibitors chemically bind to protease, so that protease cannot cleave the HIV proteins into mature viral particles FROM: http://www.thebody.com/content/art53123.html What's in the Pipeline? A Better Booster? It could be that the drugs in the AIDS pipeline with the most potential for bringing dramatic change are not anti-HIV drugs at all. Rather, they are new agents that slow the metabolism, boost blood levels, and improve the potency of certain ARVs. As of now the only pharmacokinetic (PK) enhancer on the market is ritonavir (Norvir) from Abbott Laboratories. Originally approved as an HIV protease inhibitor, the drug's metabolic inhibiting side effect turned out to be more useful than its antiviral properties, and it became an essential ingredient in Abbott's popular coformulated protease inhibitor Kaletra. However, ritonavir use has been associated with increased blood lipid levels and diarrhea. There are high expectations that new, specifically designed boosters from Gilead, Tibotec, Sequoia, and Pfizer will come with fewer unwelcome side effects. Abundant boosters should also make possible a greater variety of combination tablets and all-in-one regimens, as more companies team up to pack three drugs (plus a booster) into a single daily pill. Convenient, tolerable drugs make treatment easier to start and stick with, which leads to better long-term outcomes. With a trend to prescribing earlier in the disease and a widening campaign to test and treat tens of thousands of people who are infected but undiagnosed, these small advances can help make lifelong therapy a more palatable prospect. You might also be interested in work coming from Montreal, where they are first using Highly Active Antiretroviral Therapy (HAART) for AIDS, and then using chemotherapy to actually kill the remaining cells harboring the retrovirus. I've read a few accounts of patients whose ME/CFS has improved significantly after chemo. Again, I have no clue whether this might work with XMRV, but it's an interesting proposition. It is ironic that for a disease so maligned as "somatization", I imagine many of us might even jump at the chance of dreaded chemo, if it meant an end to this devastating disease. Check this out: Treatment of HIV 'sanctuary' cells creates path for possible cure: http://www.montrealgazette.com/story_print.html?id=1720793&sponsor= Excerpt: Though there are limits to the success of antiretroviral therapy, Routy and Sekaly say the new treatment's success will be contingent on a patient's positive response to antiretroviral therapy. If a patient shows success with current treatments, then the new treatment can target the cells, killing those last remaining ones, and "the patient will remain virus-free for a long time or forever," said Routy. Hope is a good thing.