When I began my transformation from victim to activist, I had to understand the disease process. My world had just been turned upside-down by my daughter’s diagnosis. After a period of anguished grieving, my logical side took over. I knew that with the existing IDSA party line, there was little hope for mainstream medicine to acknowledge her illness, let alone treat her. So I set out to learn everything I could about this disease, with the hope that one day, if a cure was discovered, I would be at the front of the line with my sweet, beautiful, innocent child.
Through a series of divine connections, I found my way to the LYMErix vaccine whistleblower, a former BigPharma scientist who quite honestly scared the crap out of me. In her Facebook posts she was intimidating–smart, straightforward, no bullshit. Many people interpreted her rants about sticking to the science as personal attacks. I was afraid I wasn’t smart enough to measure up, and that I risked being the object of one of these rants, but I had a feeling in my gut that I had to know this woman.
After studying her Website, www.actionlyme.org, I wrote a summary of what I understood to be the mechanisms of the disease process. I sent it to her in a Facebook message and asked her if it was accurate. She made a few minor corrections and inserted the more technical information, but what follows is the Borreliosis Basics piece that resulted. I’m also now honored to call Kathleen my friend, and I fail to find the words to describe how much respect I have for her. She is a remarkable woman and exceptional human being.
Now, chew on this:
Borreliosis is a multi-system disease caused by a spirochetal bacterium (parasite). A spirochete is a spiral-shaped parasite with a unique mechanism for movement that features a bundle of tail-like “flagella” which resides inside the cell wall.
Borreliosis is transmitted primarily through the bite of an infected tick, but also may be transmitted by insect vectors, in utero to an unborn fetus (according to Yale), and possibly via sexual intercourse. If not treated immediately with antibiotics, the infection can persist for years and cause neurological diseases such as MS, Lupus, cancer, Chronic Fatigue/Myalgic Encephalomyelitis, ALS (Lou Gehrig’s Disease) and Alzheimer’s, according to IDSA and the CDC. Thus, borreliosis is commonly referred to as “The Great Imitator” or “New Great Imitator.”
Borreliae parasites have the ability to shed (bleb off) their outer membrane lipoproteins to evade detection by the immune system in a mechanism commonly known as antigenic variation. These lipoproteins are called “outer surface proteins” (Osp) and “variable major proteins” (Vmp). In layman’s terms, the blebbing, or shedding, of OspA by the borreliae parasite sends the immune system after the OspA, allowing the spirochete to hide from immune attack and persist in the host.
Additionally, several of these outer surface lipoproteins, such as OspA (the Lyme “vaccine”–LYMErix) are TLR-2 agonists or fungal antigens, meaning they essentially disable the immune system. They do this by way of tolerance to other fungal antigens (TLR2s) as well as tolerance to other antigen types, managed by other TLRs.
See this report : “Because IRAK1 is required forTLR7/9-induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus
Exposure to shed borrelial lipoproteins causes fungal tolerance in the blood and the inability to get rid of mycoplasma/eperythrozoons from the blood, especially from the red blood cells (which causes fatigue). Also, there is cross-tolerance to TLR4 agonists from constant TLR2-agonism of shed borrelial antigens like OspA and vice-versa.
This creates an environment where opportunistic infections can thrive and cause chronic, disabling disease.
Additionally, TLR2-agonist tolerance apparently reactivates latent herpes viruses, particularly Epstein Barr Virus (EBV). (Reactivation occurs thru IL-10, and the inhibition of apoptosis of OspA or EBV-infected cells, the mechanism shown above re TLR2-signaling and the inhibition of IFN-I, and perhaps other unknown mechanisms.)
Chronic EBV is probably the main driver of all these New Great and Great Imitator diseases.