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HLA-DR alleles determine responsiveness to Borrelia burgdoferi antigens
Bettina Panagiota Iliopoulou, Mireia Guerau-de-Arellano, and Brigitte T. Huber. Arthritis Rheum. 2009 December; 60(12): 3831Nancy,thanks very much for posting this research…I’d seen the earlier study, but not the more recent, second one.
LLMDs have been saying this for years and it seems that this is now playing out in research that is indisputable:
http://www.nature.com/news/2011/110805/full/news.2011.463.html
“This finding suggests that patients with chronic symptoms have experienced a prolonged infection, caused by microbes that have evaded the immune system by varying the epitopes they carry. As a result of these variations, the body makes new antibodies targeting the modified protein. The longer the microbe manages to keep changing, the more diverse its host’s antibodies become.”
Borrelia has the unique ability to change up its outer surface proteins when under attack (by antibiotics, the immune system or any other unfriendly environmental attack). It uses this “cloaking device,” to literally evade immune surveillance as a self-protecting mechanism….not to mention reverting to dormant cystic forms that have reduced outer surface proteins and that these organisms hole up in bio-film communities, conferring protection to one another.
The really jaw-dropping part about this article is that one of the chronic Lyme denialists got the last word and still persists in the old, worn out argument that chronic Lyme is a psychosomatic illness and by telling a patient they will feel sick after taking the standard course of antibiotics, they will remain sick. Which begs the question….does this guy have a magic wand he can wave to tell his patients, “Abracadbra – you are no longer sick,” and, just as mysteriously, they won’t be? Well, maybe these guys are hoping magic will still work, as they race to find research grants (while denying other research to the peer-reviewed journals that doesn’t agree with their own), to devise their own lucrative lyme testing kits, vaccines and curative “therapies,” (for a collection of symptoms they say don’t exist, except in the chronic Lyme patient’s head). It’s an irony that these guys who persist in calling chronic Lyme a psychosomatic illness, persist in finding ways to profit from the very disease they deny is real:
“But a predictive marker won’t be useful without new therapies for the persistent symptoms, says Henry Feder Jr, a physician specializing in infectious diseases at the University of Connecticut Health Center in Farmington. If an immune response problem leads to the syndrome, antibiotics won’t help. “I guarantee you that if you tell a patient they won’t feel better after antibiotics, they won’t,” Feder says. “We need to know what’s going on.””
There are many who have passed through RBF and reached remission from “syndromes” on antibiotic therapy who are living proof that “an immune response to a syndrome,” can be reversed with abx therapy.
This debate just gets curiouser and curiouser as time goes on. I’m blown away that these guys (chronic Lyme denialists) can actually still retain any semblance of credibility in medicine, at all. It’s just unfathomable to even a feeble lay mind like mine that that the conclusions drawn from this pretty amazing research, straight out of the prestigious halls of Weill Cornell Medical College in New York, is being downplayed by a guy who seems to wield a magic wand and can just tell his patients they are well again or not. Maybe it’s just me…but it’s hard not to think you’re traveling through the twilight zone when Lyme researcher egos get in the way.
Very well said, indeed.
I’ve seen that article before, and every time I read Feder’s comment I’m stunned by his arrogance. It’s sickening.
The truth will out.
Maz – I had not seen the previous article and comments…arghhhhh!!! You’ve hit the nail on the head with your comments–very well put.
What amazes me about the article is that the authors of the study, even though they use the term ‘post-Lyme-syndrome’, don’t seem to rule out infection–they just discuss the immune response of the study paticipants.
“That could mean they naturally have a different antibody response to the infection than most people; it could mean they weren’t treated properly; or it’s possible they were reinfected and the second infection was never treated,” he says.
But, then in the last paragraph the author of the article gets the comment from Feder–what a a non sequitur!!! and of course, that will leave most readers with the anti-antibiotic stance.
My son is a classic example of chronic persistent infection in someone who is HLA dr4 positive and went for years before diagnosis. The infection is deeply entrenched and he has not yet been symptom-free. But, when we’ve taken a break from abx he gets worse…and is doing the best he’s done on continual therapy.
Nancy
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