Scientific-Breakthru-Despite-the-HHS.gov Department

Scientific-Breakthru-Despite-the-NIH Department:

Treatment for Chronic Lyme, CFIDS and MS is the same (clue; Epstein-Borreliosis):

Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders

More Scientific Evidence that the Anti-CD20 Chemo Drug Treats LYMErix-Disease (OspA > IL-10 > CD4+ >> EBV transformation)

... Remember, now: Yale wanted to give everyone a vaccine that caused cancer, in addition to MS, Lupus, ALS, etc...

Rituximab Clinical Trial Q&A, Developed by the ME Association

Follow up:

More proof that LYMErix caused the disease IDSA coined "The New Great Imitator" (OspA promotes IL-10, which suppresses CD4+ function, which controls EBV proliferation):

1) PubMed on EBV and CD20, demonstrating that Rituximab is an anti-EBV, or Anti-CFIDS, or Anti-MS, or Anti-Lupus, or Anti-Chronic Lyme drug:
http://www.ncbi.nlm.nih.gov/pubmed?term=EBV%5BAll+Fields%5D+AND+CD20%5BAll+Fields%5D&cmd=DetailsSearch

2) CD4+ T-cell effectors inhibit Epstein-Barr virus-induced B cell proliferation... [J Virol. 2001] - PubMed - NCBI "Thus, unlike the killing of EBV-infected lymphoblastoid cell lines, in which CD8+ cytolytic T cells play an essential role, prevention of early-phase EBV-induced B-cell proliferation requires CD4+ effector T cells."

The above article was cited by 16 others: http://www.ncbi.nlm.nih.gov/pubmed?db=pubmed&cmd=link&linkname=pubmed_pubmed_citedin&uid=11264363

3) Suppressed induction of mycobacterial antigen-specific Th1 CD4+ cells... [Int Immunol. 2010] - PubMed - NCBI "Our data suggest that induction of anti-mycobacterial CD4(+) T(h)1 cells is suppressed in the mycobacteria-infected lung partially by IL-10 [immunosuppressive cytokine elicited/promoted by OspA]."

4) and Allen Steere with his head up his ass, once again:
T helper 1 response is dominant and localized to the synovial fluid in patients with Lyme arthritis.
http://www.ncbi.nlm.nih.gov/pubmed/9551943

And this is in addition to the other evidence that we have of Chronic Epstein-Borreliosis.

5) Toll-like receptor agonists synergistically increase proliferation and activation of B cells by epstein-barr virus.

6) Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2.
"Ligands for TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive effect on B-cell transformation"

Cited By 6: http://www.ncbi.nlm.nih.gov/pubmed?db=pubmed&cmd=link&linkname=pubmed_pubmed_citedin&uid=17522215

7) Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells.

This is a mechanism that we did not know about before: IL-10 reducing the number of CD4+ cells, which are required to keep EBV proliferation under control. This explains why Allen Steere's Knee-Only people don't have the other fatigue and neurologic symptoms - which are due to EBV and tolerance to mycoplasma in the blood.

8) (1991) Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression.

"Interleukin 10 (IL-10) and viral IL-10 (v-IL-10) strongly reduced antigen-specific proliferation of human T cells and CD4+ T cell clones when monocytes were used as antigen-presenting cells. In contrast, IL-10 and v-IL-10 did not affect the proliferative responses to antigens presented by autologous Epstein-Barr virus-lymphoblastoid cell line (EBV-LCL). ...

"Inhibition of antigen-specific T cell responses was associated with downregulation of constitutive, as well as interferon gamma- or IL-4-induced, class II MHC expression on monocytes by IL-10 and v-IL-10, resulting in the reduction in antigen-presenting capacity of these cells. In contrast, IL-10 and v-IL-10 had no effect on class II major histocompatibility complex (MHC) expression on EBV-LCL. The reduced antigen-presenting capacity of monocytes correlated with a decreased capacity to mobilize intracellular Ca2+ in the responder T cell clones. The diminished antigen-presenting capacities of monocytes were not due to inhibitory effects of IL-10 and v-IL-10 on antigen processing, since the proliferative T cell responses to antigenic peptides, which did not require processing, were equally well inhibited. Furthermore, the inhibitory effects of IL-10 and v-IL-10 on antigen-specific proliferative T cell responses could not be neutralized by exogenous IL-2 or IL-4. Although IL-10 and v-IL-10 suppressed IL-1 alpha, IL-1 beta, tumor necrosis factor alpha (TNF-alpha), and IL-6 production by monocytes, it was excluded that these cytokines played a role in antigen-specific T cell proliferation, since normal antigen-specific responses were observed in the presence of neutralizing anti-IL-1, -IL-6, and -TNF-alpha mAbs. Furthermore, addition of saturating concentrations of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha to the cultures had no effect on the reduced proliferative T cell responses in the presence of IL-10, or v-IL-10. Collectively, our data indicate that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.

9) "All gammaherpesviruses express homologues of antiapoptotic B-cell lymphoma-2 (BCL-2) to counter the clearance of infected cells by host antiviral defense machineries." http://www.ncbi.nlm.nih.gov/pubmed/18248095

▲This is in addition to the Bb and OspA-induced elevated IL-10, which suppresses CD4+ cells, which are needed to keep the EBV infection under control.
This is in addition to possible other unknown mechanisms by which fungal infections help viral infections along to unlatency...
One of which, we think, is the inhibition of apoptosis of Bb-infected cells or the inhibition of B-cells to apoptosis after "reprogramming" by OspA-like antigens:

2003, NIH on OspA "reprogramming immunity" http://www.jimmunol.org/content/170/1/508.full
inducing tolerance to other fungal infections in the blood.

Remember, now. Lyme is considered to be a bioweapon. See BIOWEAPONS_ATTRIBUTES.htm and

"The Army says ticks could be used to spread diseases." - Poughkeepsie Journal.
This is why the CDC and the Israeli/ALDF Lyme crooks keep trying to spin the disease as the arthritis-only in the journals.

10) NIH says the treatment for Chronic Fatigue-Lyme-MS is probably something like Acyclovir and anti-CD20 Leukemia drug, followed by Stem Cells:

Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States.
http://bloodjournal.hematologylibrary.org/content/117/22/5835.long

And:

Dr. Montoya's team enrolled 30 patients with elevated levels of antibodies against Epstein-Barr virus and HHV-6, a herpes virus, in a trial and treated them with valganciclovir, an anti-viral medicine. Dr. Montoya says patients on the drug showed improvement in cognition and fatigue.
http://online.wsj.com/article/SB10001424052748703858404576214443015558976.html

What about the tolerance to mycoplasma, you may say to yourself...

http://www.ncbi.nlm.nih.gov/pubmed?term=%28%22mycoplasma%22%5BMeSH+Terms%5D+OR+%22mycoplasma%22%5BAll+Fields%5D%29+AND+CD86%5BAll+Fields%5D&cmd=DetailsSearch
Rituximab is anti-CD20 monoclonal antibodies. But what is the anti-CD86 monoclonal antibody marketed as, for instance?
"Two tumor cell supernatants, MDA468 and 293T, were found to be able to affect the in vitro differentiation of DCs from monocytic precursors, leading to the generation of a distinct type of DC with markedly reduced expression of DC-SIGN, downregulation of CD11c, HLA-DR and CD1a, and upregulation of CD123, HLA-ABC, CD80, CD40, CD86, CD54, CD83, CD25 and CCR7. Functionally, these DCs exhibited reduced phagocytosis and enhanced allostimulatory capacity." http://www.ncbi.nlm.nih.gov/pubmed/15864737

Mycoplasma-mediated alterations of in vitro gen... [J Biomed Sci. 2005] - PubMed - NCBI

I am sure it is not just CD86, in other words. But what else? 54? 25? Etc.

" Dr. Montoya's team enrolled 30 patients with elevated levels of antibodies against Epstein-Barr virus and HHV-6, a herpes virus, in a trial and treated them with valganciclovir, an anti-viral medicine. Dr. Montoya says patients on the drug showed improvement in cognition and fatigue.
http://online.wsj.com/article/SB10001424052748703858404576214443015558976.html

‎
The NIH says (Steve Straus, the CFIDS's patients Nemesis, now dead, thank God):

"Although patients with CAEBV from Japan have normal or increased numbers of NK cells, many of our patients had reduced NK-cell numbers. ***Although immunosuppressive agents, rituximab, autologous cytotoxic T cells, or cytotoxic chemotherapy often resulted in short-term remissions, they were not curative. Hematopoietic stem cell transplantation was often curative for CAEBV, even in patients with active lymphoproliferative disease that was unresponsive to chemotherapy.*** These studies are registered at http://www.clinicaltrials.gov/ as NCT00032513 for CAEBV, NCT00062868 and NCT00058812 for EBV-specific T-cell studies, and NCT00578539 for the hematopoietic stem cell transplantation protocol.
The NIH says ▲ Stem Cells is the treatment for chronic EBV, but then again, this is the NIH and Steve Straus (allegedly, since he is dead);

We can trust the NIH as far as we can throw them.

With transplant patients, there is always the problem of EBV-related cancers:

New: "NIH scientists outline steps toward Epstein-Barr virus vaccine
"Organ transplant recipients and people infected with HIV (who become infected with or who already are infected with EBV) also may develop EBV-associated cancers."
Because they're ▲ given immunosuppressive drugs, which is the same thing as having a tolerance to mycoplasma in the blood, which is what we Chronic Lyme/Chronic Fatigue victims have acquired.

New: "Understanding kiss of death for some improves outlook for others"

11) NIH SAYS LYMERIX (Pam3Cys) ACTIVATES VIRUS REPLICATION:

http://www.jleukbio.org/content/75/3/460.long

The induction of Toll-like receptor tolerance enhances rather than suppresses HIV-1 gene expression.

12) Influence of Coinfecting Pathogens on HIV Expression: Evidence for a Role of Toll-Like Receptors¹

"The above findings point to TLR2 agonists [from fungi like OspA or tuberculosis] as the major stimulus of HIV gene expression in this animal model of mycobacterial coinfection. Interestingly, TLR2 has been shown to play only a limited role in in vivo control of mycobacterial infection in murine infection models (52, 53, 54, 55)."
http://www.jimmunol.org/content/172/12/7229.full

The NIH says ▲ you can't use mice as a model of Lyme or LYMErix-disease and that such fungal infections as Tb or OspA from Lyme Relapsing Fever help activate viruses.

One hopes the new Mouse Factory under development as an excuse for research science at Yale and UConn (donated by the State of Maine) remembers that the transgenic Lyme mice must have human TLR2, for starters. Not too many people associated with Connecticut, UConn or Yale read, however.

Maybe the Maine Mouse Plant will also export some Maine people who can read to them.

13) "This process, which was initially termed "endotoxin tolerance", refers to the induction of a hyporesponsive state in macrophages following primary exposure to microbial ligands such as lipopolysaccharide (LPS), bacterial lipoprotein, lipoteichoic acid, and oligo CpG–DNA, now known to signal through TLRs. The resulting tolerant state is associated with a marked decrease in proinflammatory cytokine production following secondary challenge with these ligands [111213 ]."
http://www.jleukbio.org/content/75/3/460.long

More Fungal (OspA-induced)-Viral Synergism AKA Chronic Lyme/the New Great Imitator outcomes of it:

14) Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection
http://jem.rupress.org/content/205/2/323.full

The above means: We Chronic Lyme victims could possibly become walking bacterial-viral nurseries. If ever there is a new pandemic, be it influenza or whatever, it will probably develop in the chronic Lyme/Fibromyalgia/Chronic Fatigue community. But we'll all be spared, since we're immune suppressed.

Thankfully, LYMErix was removed from the market due to all the adverse events that resulted in a Chronic Lyme-like illness (see SmithKline's Dennis Parenti admit to it, below); LYMErix vaccinations would have increased the population of pandemic disease nurseries on two legs.

The CDC diagnostic standard - the falsified Dearborn case definition - of course, continues to increase the population of walking immune-suppressed/fungal-viral nurseries. The ongoing, unprosecuted crime of Dearborn increases the likelihood that a host will encounter/grow disease variants that doesn't kill them... but will be The Pandemic.

15) Characteristics of Epstein-Barr Virus Envelope Protein gp42
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854865/?tool=pubmed

The major cellular event in viral infection is the delivery of the viral capsid or nucleoprotein core into the host cell cytoplasm. Enveloped viruses such as the herpesviridae perform this delivery by fusion triggered by viral cell envelope glycoproteins binding to receptors on the host cell membrane. The EBV genome encodes several glycoproteins required for fusion and entry into host cells. Glycoprotein B (gB), gH and gL are necessary for fusion in both epithelial and B-cells [12–22], and glycoprotein 42 (gp42) is required for B-cell fusion but is inhibitory for epithelial fusion [23–26]. Gp350/220 serves as the first viral attachment glycoprotein for B-cells through binding to complement receptor type 2 (CD21) but is not required for entry [27]. Following this attachment, viral fusion is triggered by the binding of gp42 to human leukocyte antigen (HLA) class II receptor [28–30]. When gp42 binds to this receptor, it blocks recognition of the complex by T-cell receptors [31], possibly helping the virus to escape immune system detection.

- - - - - - - -

People ask me all the time, "What does this all mean and what is next?"

And I have to say, "I don't know. We're dealing with the CDC and the NIH. It's been longer than any of us can remember (1980s), that the NIH ever made any sense, if ever. "