Ali and I started antiretroviral therapy a year ago. We both improved noticeably for the first nine months, though the treatment didn’t prevent our crashing when we started to engage life again. My setback was brief and I seem to be able to push the envelope a little now without crashing in a prolonged way. Ali has had a tougher time of it. In the last few months tachycardia became a serious problem, not new, but worse, and she started atenolol. It helped with the tachycardia, but some new symptoms started. She ended up stopping atenolol and AZT at close to the same time a month ago, to see if they were making things worse. Stopping the atenolol clearly helped, stopping AZT less clearly so, but the tachycardia does seem to be subsiding and in the last week or so, she seems to be on an upswing. Although she has been homebound for a couple of months, she is feeling like she can go out again. She has been writing productively throughout. I also stopped AZT a couple of weeks ago. I was wondering if maybe I’m a little weaker than a year ago though my CPK is fine and who can tell? But AZT is the most problematic of the drugs long term and there is no way at this point to evaluate whether it is worth it or not. I didn’t notice anything coming off it. We continue on Viread and Isentress. When I think about stopping them, I remember the fifteen years of malaise I endured, now mostly gone, and the intense neuropathy pain that is now little more than background noise.
Under the best of circumstances, the drugs available to us based on in vitro studies (reverse transcriptase inhibitors and an integrase inhibitor), are an incomplete solution, as they can only control early stage replication events. Patients who have been sick for a long time most likely have a large amount of integrated virus cranking out viral product and fueling persistent immune activation. The drugs we have will not affect this, only preventing infection of new cells. Also we do not have a protease inhibitor to prevent assembly of new viral particles. The HIV protease inhibitors were ineffective against XMRV in vitro in the Singh study. XMRV protease is not the same as HIV’s. Crystal structure of XMRV protease differs from the structures of other retropepsins. Dimaio
I would like to restate that this blog is personal and not endorsed by the WPI. It precedes the association. The opinions expressed here are mine alone. I am working for the WPI in an administrative capacity, recruiting, planning the clinic to meet the needs of patients, fielding questions. My job is to create an environment where the best possible care can be provided and implement the clinical database. Organizing, creating a framework, but no one need be concerned that I will be setting medical policy based on my own opinions. Medical decision making will of course occur within the context of individual physician patient relationships. We are gathering a network of physicians to work at a distance with the clinic doctors and over time we will work towards consensus.
“Cover-up” in my last post refers to people who have been wrong and now don’t want that to come to light. I was not trying to suggest that there was or is a conspiracy in the sense that people are planning with each other to do dastardly deeds. My interest in the dangers of vaccines has nothing to do with conspiracy theories. It has to do with the very strong anecdotal evidence that vaccines have harmed a lot of people in the various neuroimmune disease cohorts, ME/CFS, ASD, GWI. If you listen to many histories, there is a clear suggestion that vaccination is one of the major triggers for X related disease. Whether the reason for that is the immune challenge or the introduction of a retrovirus, it seems prudent for the moment to refrain from administering vaccines which are not immediately necessary until we know more. We need to be sure that we aren’t putting patients at more risk from vaccinations than they are from the diseases for which they are being vaccinated. There has always been an element of the vaccination program that sacrifices a few individuals for the greater good, but this seems higher than a small statistical risk for this group of patients. It’s strange that this is such a controversial thing to say. Seems like a no brainer to me. Primum non nocere.
Like everybody, I’ve wondered a lot about where XMRVs came from. I’ve been thinking about the ideas in my last post, reading widely for some time, but my thoughts coalesced when I read the Paprotka CROI abstract. Frankly, I was expecting that people far more knowledgeable than I would punch holes in what I’d written. But it has now been read by thousands of people including a bunch of virologists and although some found it inflammatory, nobody has yet taken exception with the science. Pretty scary. If my hypothesis turns out to be correct, we’ve given retroviral evolution a leg up by a couple of hundred thousand years or so in less than a century. And seriously weakened the health of the species. So let’s hope I’m wrong.
Good doctors must engage in inductive reasoning. Educated guess. There may be much unknown, but there is still a real patient sitting there in need of treatment. Scientists argue that they must go through all the necessary deductive steps to get to the solution. That leaves a lot of patients with no meaningful treatment. In an emergency, it’s a good idea to skip to the answer if you can, figure out what you can do and fill in the blanks later. It’s pretty clear we have a public health emergency. Whether the etiology of the illness is X, Y or Z, it is retroviral in origin. It fits like a glove, better than anything else ever has. Making that leap allows one to think about the illness in a way that doesn’t yet offer a cure, or even a functional cure, but it does help in the choices of useful or palliative therapies. Most importantly, it should help us not to hurt the patients. Huge damage has been done because of ignorance. At least we can put an end to that.