Once we understand what the disease is, the next question, invariably, is, “what’s the treatment?” Thank you, MontanaNAR, for raising the question. These reports were compiled by Kathleen, of ActionLyme. She says:
Read these 4 reports, all new, and see that the treatments for HLA-associated sepsis outcomes (MS, Lupus, maybe RA… and are reactivated herpesviruses), are the same as non-HLA-linked sepsis outcomes (Chronic Fatigue, Chronic Lyme, fibromyalgia…also reactivated herpesviruses and etc, like the NIH says here.
Stem cells, immune boosters, B cell depletion (Rituximab), some say add antivirals…
The NIH also says all this occurs as a result of exposure to TLR2-agonists like fungi, like Lyme and LYMErix… The NIH says in the NYTimes that Chronic Lyme is really about reactivated EBV/similars, summer of 2013. And Paul Duray was also an NIH employee, which, as you can see in the header graphic for this group speaks about Lyme causing something like a leukemia (“EBV-transformed cells”).
The last report (new) shows the same dynamic in parallel in oral infections.
FROM THE NIH, Dec, 2014
”Stem cell transplants may halt progression of multiple sclerosis”
Three-year outcomes from an ongoing clinical trial suggest that high-dose immunosuppressive therapy followed by transplantation of a person’s own blood-forming stem cells may induce sustained remission in some people with relapsing-remitting multiple sclerosis (RRMS). RRMS is the most common form of MS, a progressive autoimmune disease in which the immune system attacks the
brain and spinal cord. The trial is funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (ITN) .
Three years after the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant or HDIT/HCT, nearly 80 percent of trial participants had survived without experiencing an increase in disability, a relapse of MS symptoms or new brain lesions. Investigators observed few serious early complications or unexpected side effects, although many participants experienced expected side effects of high-dose immunosuppression, including infections and gastrointestinal problems. The three-year findings are published in the Dec. 29, 2014, online issue of JAMA Neurology.
“These promising results support the need for future studies to further evaluate the benefits and risks of HDIT/HCT and directly compare this treatment strategy to current MS therapies,” said NIAID Director Anthony S. Fauci, M.D. “If the findings from this study are confirmed, HDIT/HCT may become a potential therapeutic option for people with this often-debilitating disease, particularly those who have not been helped by standard treatments.”
FROM THE NIH, AGAIN:
“Preventing Secondary Infections”
“Some people who survive sepsis can develop secondary infections days or even months later. A research team
that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy
people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]
***** Of the three study groups, people with sepsis had much higher levels of these viruses, suggesting reactivation due to compromised immune responses. Immune suppression could make it difficult
to defend against the reactivated viruses as well as new infections like pneumonia. The team now plans to test whether immune-boosting drugs can prevent deaths in sepsis survivors.****
This Inside Life Science article was provided to Live Science in cooperation with the National
Institute of General Medical Sciences, part of the National Institutes of Health.
Older Patients have the same kind of immune system as people with Lyme or LYMErix disease since Old People’s immune systems are CHARACTERIZED by crappy TLR2-agonist responses
NEW, Upenn, Oral infections…
Notice this dynamic is identical to the one we propose with OspA/shed fungal antigens from Borrelia (TLR2-agonists) turning off the immune response, allowing the secondary infections (in our case, EBV, etc) to do all the damage (and not always inflammation, BTW);
And it is the same as the NIH’s Sepsis dynamic in the above 3 articles…
Clearly points to something like OspA as the culprit (TLR2-agonism):
“P. gingivalis uses this connection between C5aR and TLR2 to disarm and dissociate the MyD88 pathway, which normally protects the host from infection, from the proinflammatory and immune-evasive pathway mediated by Mal and PI3K,” Hajishengallis said.
So, the NIH and some other researchers are on it, but until OspA disease is recognized for what it truly is, we Lyme/LYMERIX victims will have difficulty accessing the treatments.