But I've heard they've been making progress lately, and what with the GEAS report, I'm feeling more obliged to dip my toes back into the information stream. Maybe I'm just adding to the rampant speculation, but I'm wondering if ReDS has biologicals similarities to other diseases.
A friend of mine once came down with a case of chronic Lyme's disease, and an article she sent me a long while ago made me wonder if ReDS works by a similar mechanism. Chronic Lyme's disease, is different than regular Lyme's disease, by the way. It doesn't always show up on normal tests for Lyme's because the bug hides so well. And the symptoms can be like Chronic Fatigue Syndrome (a controversial beast itself).
Anyway, so what happens is the Lyme's bug hides out in places where the immune system doesn't think to look. Also it is able to shift itself into different forms to avoid antibiotics.
Article excerpt:
Once disseminated throughout the body, B. burgdorferi secludes itself and becomes difficult to detect through laboratory testing—and by the host’s immune system. The bacterium may hide in its host’s WBCs or cloak itself with host proteins. Furthermore, it tends to hide in areas not usually underimmune surveillance, such as scar tissue, the central nervous system, theeyes, and deep in joints and other tissues.
Phase and antigenic variations allow B. burgdorferi to change into pleomorphic forms to evade the immune system and antibiotics. The three known forms are the spiral shape that has a cell wall, the cell-wall-deficient form known as the “L-form” (named not for its shape but for Joseph Lister, the scientist who first identified these types ofcells), and the dormant or latent cyst form.
Encapsulating itself into the inactive cyst form enables the spirochete to hide undetected in the host for months, years, or decades until some form of immune suppression initiates a signal that it is safe for the cysts to open and the spirochetes to come forth and multiply. Each of these forms is affected by different types of antibiotics. If an antibiotic targets the bacterium’s cell wall, the spirochete will quickly morph into a cell-wall-deficient form or cyst form to evade the chemical enemy.
Yikes. Is this why ReDS is so intractable? Has it learned to be a superbug? In that case, developing a simple vaccine or antibiotic regimine probably isn't in the cards.
This will take some serious nanoengineering and machine learning to crack.

