You know how much I hate to be the one to tell you:
UCal, San Francisco:
“Early Lyme disease prior to antibiotic therapy was characterized by marked upregulation of Toll-like receptor signaling but lack of activation of the inflammatory T-cell apoptotic and B-cell developmental pathways seen in other acute infectious syndromes,” wrote the study’s authors. “Six months after completion of therapy, Lyme disease patients were found to have 31 to 60% of their pathways in common with three different immune-mediated chronic diseases. No differential gene expression signature was observed between Lyme disease patients with resolved illness to those with persistent symptoms at six months post-treatment.
“Six months after treatment, 15 of the 29 patients in the study had fully recovered, while 13 had persistent symptoms, and one had dropped out. Despite the stark differences in how the patients reported feeling, the researchers could not detect transcriptional differences between the two groups. They said larger studies are needed to confirm this finding.”
UCal, Davis and Immunosuppression and Borrelia living in the lymph nodes with EBV.
And like we have been telling you for the last 10+ years, and calling it “fungal-viral synergy,” and proving that ILADS’s various, never-ending tall tales (like “biofilms”) about why they are not curing you is a lie they really ought to give up. Lyme and LYMErix are B cell mutations or diseases, and getting rid of spirochetes or whatever else with antibiotics will not restore your health:
“Infection with B. burgdorferi suppresses the generation of protective IgG responses to influenza vaccination.
“Consistent with the strong induction of early extrafollicular B cell responses to Bb-infection, no significant differences in the magnitude or isotype-profile were observed for influenza-specific ASC IgG antibody production in the lymph nodes on day 10 after infection between vaccinated and vaccinated and Bb-infected mice, as determined by ELISPOT analysis (Fig 6B). The frequencies and absolute numbers of activated HA-specific (TS1+) CD4+ T cells, as measured by induction of ICOS, a co-stimulatory molecule critical for GC B cell responses, was also similar in both groups of mice (Fig 6C and 6D). And finally, serum IgG responses to A/PR8 over the first 3 weeks of infection showed no difference compared to the vaccine-treated only mouse group. Thus the early antibody response to both Bb and to the co-applied vaccine appeared strong.
“However, dramatic differences in the antibody responses to the influenza vaccination became apparent by about four weeks of infection. A/PR8-specific IgG responses plateaued around this time in the Bb-infected group, while they continued to rise in the vaccinated-only group, resulting in serum IgG levels at that were greatly higher compared to the titers seen in the Bb-infected and vaccinated group after 4 weeks until study end (26 weeks; Fig 6E). The lack of serum IgG responses in the Bb-infected mice might have been due to the reduction in bone marrow ASC by 9 weeks of vaccination/infection compared to the vaccine-only group (Fig 6F).
“To determine whether the Bb-infection-induced changes to the B cell response induced to the influenza vaccination had a functional effect on the protective capacity of the vaccine, we conducted passive protection experiments. Remarkably, when naïve mice received immune serum from mice either Bb-infected or not and then vaccinated with influenza antigens, only mice receiving serum from flu-vaccine-only mice were protective from clinical signs of disease after influenza virus challenge (Fig 7). We conclude that Bb-infection suppresses the induction of long-term protective immunity to a co-administered vaccine antigen.
“The studies here focused on B cell responses to Bb induced in the lymph nodes, as we found Bb spirochetes by culture and by histology as early as 24h after infection . While the lymph nodes then remained culture positive throughout the infection, the spleen was largely culture negative . The reasons for this lack of splenic involvement during disseminated systemic Bb infection that would be expected to result in antigen presentation and immune response induction also in the spleen are unclear. Interestingly, a study on Ehrlichia muris infection, another tick-transmitted disease, similarly noted the absence of splenic involvement in the immune response to both E. muris and a co-administered model antigen, but found lymph node responses to be unaffected .
“From these results we propose a model of Bb immune evasion in which the accumulation of live Bb in lymph nodes causes changes in tissue structure and a rapid expansion of their cellularity [20,21]. The presence of Bb, which is known to express numerous complement-inhibitory proteins [7,8], including a C4b-binding protein , or the ensuing inflammation of these tissues, may result in a reduction in local complement C4 deposition on the FDC, which is indicated by the lack of staining for C4 deposition on FDC (Fig 4 and S1 Fig). While speculative at this time, it is possible that a lack of antigen-C4 deposition diminishes antigen-presentation by the FDC to GC B cells. Reduced antigen-presentation could result in the premature collapse of the GC responses, which we have demonstrated here and previously [20,22,28]. We hope to test this model in the future.”
When will you be convinced?
[see also “Borrelia surviving in the bone marrow“]: