09 Feb 2012 

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Pharma/CDC on Brain damage from vaccines, Fauci, Phages, Bioweapons manufacture

HHS.gov is Incompetent; BMJ calls fraud "crime.")

Official: CFIDS and MS-Lyme are the same disease; Epstein-Barr 


CDC Greed (won't answer the FOIA)

ELISA = arbitrary cutoff.

Disclaimer

Overview
 

TUSKEGEE - By Jerry Leonard

1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.

Bush/Gore  Oil/War-(Oct,2000)  

Bush's own explainer (Oct 2000): Iraq Oil

Iraq was an oil-theft war.

"What was discussed at a closed session of the U.S. House of Representatives? Tuesday March 25, 2008 7:37pm EST"

Theorists wrote "Not only did members discuss new surveillance provisions as was the publicly stated reason for the closed door session, they also discussed: The imminent collapse of the U.S. economy to occur by September 2008, the imminent collapse of US federal government finances by February 2009, the possibility of Civil War inside the USA as a result of the collapse and advance round-ups of "insurgent U.S. citizens" likely to move against the government.

Also theorised was the detention of those rounded-up at "REX 84" camps constructed throughout the USA and the possibility of retaliation against members of Congress for the collapses and the location of "safe facilities" for members of Congress and their families to reside during expected massive civil unrest

 

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Rockefellerian Pax AmeriTardation ◄ American White-boy Losers are such stupid losers because they're so frickin cowardly. 

European/G7 bailout?  Impossible

Canadian debt clock (private estimate)

French public debt clock

Germany's debt clock (at the top of the page)

Japan's national debt

Japanese Debt Clock (In Ten Thousand Yen Units)

Riksgäldskontoret - the national debts of Sweden

UK public debt clock

There is no sovereign wealth for Europe to bail out its banks.  This bailout is a hoax.
.

The scale of the debt crisis- (the IMF is very dangerous)

 

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◄LYMErix vaccination Scam (interview/YouTube; Sequence of events confirmed by Karen Forschner in the last Sue Vogan Show)

◄Notes from my summer 1999 conversation with Dennis Parenti, when he told me how to report adverse events to LYMErix.

 

"Astute Clinician" (Steere) to lecture at NIH - 3 Nov 1999  ◄ You will notice that this was 1999, when I talked to Dr. Dennis Parenti, who informed me about the VAERS or the FDA's Vaccine Adverse Events Reporting System, that led to the FDA's Jan, 2001 hearing on LYMErix, wherein I informed the FDA about what happened with the diagnostic standard, and that no one who attended the Dearborn conference agreed with Allen Steere (meaning it was not a consensus conference).
 

Dickson explains to FDA about the Lyme Crymes, Jan, 2001

Full 30 pages of my complaint to FDA, including pages from the Dearborn booklet, including Dressler/Steere.

Pages out of the Dearborn booklet that the FDA did not scan in.

Karen Forschner discovers Lyme Toxin (OspA)

 

Notice that all of this had absolute ZERO to do with Pam Weintraub.


So, you may say to yourself, how the hell did Pam Weintraub ever think she could claim to have solved the Lyme crimes?  She's a journalist, not a scientist.  Journalists are, sort of, parasites, if you know what I mean; they're not scientists. 

If journalists had the same abilities as scientists, they would have explained to us how the WTC7 fell down in 7 seconds- a physical impossibility unless thermate was in there on September 10, 2001.

See.  There's a huge difference between observers or commentators and people who actually do stuff.  One stupidism here is that apparently Pam Weintraub thought I would not be able to prove the series of events.

And even stupider stupidism, of course, is a vaccine for relapsing fever- thunk up by Crazy Eddie McSweegan at the NIH (but thunk up while he was employed by the US Navy).  You will not find any published scientific journal articles authored by Edward McSweegan that has to do with actual lab experimentation.  People (PhDs) who were as scientifically inept (as Crazy Eddie McSweegan) at Pfizer are "promoted" to management positions - just like Crazy Eddie - to get them out of the lab. 

You can get a degree in chemistry or physics or engineering by being good at math, for instance, but that does not imply true scientific talent. 

A real scientist never lies.  That happens to be the definition of a scientist- one who NEVER LIES.

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Well, then.  Today is among the biggest no-news days since Scooter Libby was pardoned.

Twilight of US Supremacy

Status of Other States-  Iraq doing good.

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The Wall Street Coup and the Bailout Scam
http://mrzine.monthlyreview.org/hossein-zadeh111008.html
by Ismael Hossein-zadeh

The "rescue" plan is not only fraudulent, it is also the wrong medicine for the ailing economy.

The Wall Street took the US (and the world) hostage and extracted a heavy ransom.  But while the enormous ransom was successfully extracted, there are no guarantees that the hostages will be set free from the shackles of trickle-down economics.  On the contrary, there are strong indications that the fraudulent (and perhaps criminal) bailout may turn the current crisis into a protracted agony of a long-bleeding economic depression.

Why the Bailout Scam Is More Likely to Fail than to Succeed

The bailout scam is doomed to fail because it avoids diagnosis and dodges the heart of the problem: the inability of more than five million homeowners to pay their fraudulently inflated mortgage obligations.

Instead of trying to salvage the threatened real assets or homes and save their owners from becoming homeless, the bailout scheme is trying to salvage the phony or fictitious assets of Wall Street gamblers and reward their sins by sending taxpayers' good money after the gamblers' bad money.  It focuses on the wrong end of the problem.

The apparent rationale for the bailout plan is that, while the injection of tax payers' money into the Wall Street casino may not be fair, it is a necessary evil that will free the "troubled assets" and create liquidity in the financial markets, thereby triggering a much-needed wave of lending, borrowing, and expansion.

There are at least five major problems with this argument.

The first major problem is that the current financial disaster is not really a liquidity problem as it is repeatedly portrayed to be.  It is a problem of faith and trust, or lack thereof, which in turn stems from the disproportionately large amount of junk assets or mortgages relative to real assets.  It is true that lending and credit expansion has almost come to a halt and, in this sense, there is a serious liquidity crisis.  But this illiquidity is not really due to a lack of good money or real assets in the system.  It is rather because owners of such valuable assets are unwilling to lend their precious possessions to owners of troubled assets, or worthless papers.

As Herman E. Daly, University of Maryland economist, puts it, "The value of present real wealth is no longer sufficient to serve as a lien to guarantee the exploding debt.  Consequently the debt is being devalued in terms of existing wealth.  No one any longer is eager to trade real present wealth for debt even at high interest rates.  This is because the debt is worth much less, not because there is not enough money or credit."

The second major problem with the bailout scheme is that it is simply unfeasible and ineffectual because there is just not enough good money to redeem all the bad money that has ballooned or bubbled to a multiple of the good money and/or real assets.

The initial $700 billion bailout money falls way short of what is needed to rescue the Wall Street gamblers, as it is only a fraction of their accumulated bad debt.  According to a September 29 Washington Post report:

Twenty of the nation's largest financial institutions owned a combined total of $2.3 trillion in mortgages as of June 30.  They owned another $1.2 trillion of mortgage-backed securities.  And they reported selling another $1.2 trillion in mortgage-related investments on which they retained hundreds of billions of dollars in potential liability, according to filings the firms made with regulatory agencies.  The numbers do not include investments derived from mortgages in more complicated ways, such as collateralized debt obligations.

These three categories of mortgage-related financial instruments add up to a $4.7 trillion obligation for the twenty largest financial institutions.  This is nearly seven times as large as the initial Paulson/Bernanke bailout plan of $700 billion, which means the plan is destined to be ineffectual.

Nationwide, the ratio of bad to good money is much higher.  According to Herman E. Daly, "Financial assets have grown by a large multiple of the real economy -- paper exchanging for paper is now 20 times greater than exchanges of paper for real commodities."  This means that the initial $700 billion bailout fund is simply a drop in the sea of bad debt, and that, therefore, there is not enough good money to pay for the mountain of junk assets accumulated by the gambling financial institutions.

The third major flaw of the bailout plan is that, as mentioned earlier, it does not address the real problem: the problem of rescuing the financially distressed homeowners.  As Dr. Paul Craig Roberts points out, "the Paulson bailout does not address the core problem.  It only addresses the problem for the financial institutions that hold the troubled assets.  Under the bailout plan, the troubled assets move from the banks' books to the Treasury's.  But the underlying problem -- the continuing diminishment of mortgage and home values -- remains and continues to worsen."

Simply moving soured assets from fraudulent lenders to the Treasury, that is, buying junk mortgages at face value, will neither help the millions of homeowners facing homelessness, nor help mitigate the raging financial crisis.  The bailout should, instead, focus on defrauded homeowners and real assets, not fictitious capital and its unscrupulous owners.

Instead of trying to salvage a mountain of soured assets and prop up bankrupt institutions, the government should allow for a market cleansing, or destruction, of such worthless assets by purchasing the threatened mortgages not at their inflated face value but at the current, depreciated, or market value -- as the FDR government did in response the Great Depression of the 1930s.

This alternative, homeowner-based solution would have a number of advantages.  First, and foremost, it would help citizens facing the specter of homelessness stay in their homes by allowing them to pay affordable mortgage installments based on reduced or realistic home prices.

By the same token, this solution would also allow the government to gradually recover the market-based home prices it would be paying the troubled commercial mortgage holders.  Obviously, this means that, instead of the predatory banks and similar financial institutions, the government would now be the title holder of the rescued homes -- of course, until such homes are paid for, upon which time the homeowners would take the possession of their home titles.

By cleansing the market of the dead weight of tons of junk assets, and allowing threatened homeowners to pay affordable mortgage installments, this bottom-up solution would also help restore faith and trust in the financial system, and in the lending and borrowing mechanism -- thereby also mitigating the liquidity crisis.

Furthermore, by bailing out homeowners (and real assets) instead of Wall Street gamblers, the government would need only a fraction of the money needed to pay for the huge bubble of the junk assets that have ballooned on top of a much narrower base of real assets.  Compared with the scandalous Paulson/Bernanke bailout scheme, this means that the government would end up with enough excess money to invest on a long-term, robust stimulus plan a la the New Deal of the 1930s.

And this brings us to the discussion of the fourth major problem of the Paulson/Bernanke bailout scam: lack of any economic stimulus plan, which is badly needed for economic revival.  While government substitution for predatory lenders and the resulting institution of realistic or devalued mortgage installments will certainly lighten the financial burdens of the economically-pressed, it will not relieve them from the need to earn an income and make a decent living.  Nor would it (by itself) provide the badly needed purchasing power or necessary demand to stimulate the economy.

To achieve such broader socio-economic objectives requires no less than duplicating (and perhaps even going beyond) FDR's New Deal reform package that proved critical in ending the Great Depression of the 1930s.  A comprehensive long-term public investment in both social and physical infrastructure (health, education, roads, bridges, levees, schools, green energy, etc.) is bound to create jobs, inject purchasing power and liquidity into the economy, and revive production and expansion.

Of course, such an urgently needed comprehensive investment in the future of our society requires extensive public financing, which, in turn, requires a careful and socially responsible fiscal policy.  And this brings us to the fifth major problem of the Paulson/Bernanke bailout scheme: absence of any mention, let alone change, of our warped or lop-sided fiscal policies and priorities.

The sad and sick status of our public finance (the rising budget deficits, the soaring national debt, the curtailment of crucially important social spending, and the resulting neglect of both social and physical infrastructure) is a direct consequence of our warped fiscal policies that give priority to the interests of the super rich at the expense of everybody else.  It is a direct result of the looting of our public money through a combination of (a) huge "supply-side" tax cuts for the wealthy and (b) drastic increases in the share of military spending at the expense of non-military public spending.

In a real sense, the current financial meltdown is a logical outcome of an economic philosophy that promotes extreme social inequality.  Contrary to "expert" punditry and popular perceptions, it is not simply due to personal greed; more importantly, it is the result of a systemic failure, or the outcome of the diverging and conflicting class interests.

Progressive taxation, social spending, New Deal reforms, and the War on Poverty were designed not only to protect the poor and working people against the woes and vagaries of market mechanism, but also to save capitalism from itself.  Instead of viewing public spending on social safety net programs as long-term investment in the future of the nation, trickle-down economic philosophy views such expenditures as overheads that need to be cut as much as possible.

To this effect, proponents of this philosophy have since the early 1980s been working very hard to cut taxes for the wealthy, to cut non-military public spending, and to reverse most of the social safety-net programs that were put in place by FDR's New Deal and LBJ's War on Poverty.

Not surprisingly, the result has been an extreme concentration of national riches and resources in fewer and fewer hands, side-by-side with a steady deterioration of the living conditions of the overwhelming majority of our citizens.  Unable to make ends meet, most of our citizens exceedingly resorted to borrowing.

Predatory lenders proved to be both creative and merciless in taking advantage of the economically vulnerable, or the legitimate aspirations and dreams of homeownership.  Unfettered by the irresponsible government deregulation policies, these rapacious lenders pushed loans, engaged in deceitful or fraudulent lending practices, and unscrupulously invented many shady financial instruments that resulted in the accumulation of massive amounts of fictitious assets that proved unviable, and eventually collapsed under their own dead weight.

Unless the lopsided national priorities and perverse fiscal policies, known as trickle-down or neoliberal economics, which began under Ronald Reagan, are rectified, and the resulting financial resources are invested through a broad and carefully crafted plan of social and economic recovery, no bailout plan of the plutocrats, by the plutocrats, for the plutocrats can succeed in reversing the current cycle of economic decline.

 

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NY class action ◄ Pam Weintraub's falsehoods (by omission and commission) demonstrate that Lyme victims can and should sue the State of New York rather than Corrupticut, even though Corrupticut's Yale staff Fikrig and Flavell hold the main patents and wrote the reports that demonstrate the crime (Bb-specific flagellin and the LYMErix patent).

In addition, while Pam Weintraub threatened to sue one of my Team C team members for committing a TRUISM, such a lawsuit would bring the truth of the Lyme crymes into "court," upon which, whatever "judge" that hears the case will have to refer IDSA/ALDF to a criminal court for prosecution.  It will be over the falsification of the diagnostic standard of Lyme by Allen Steere in Europe.  We will find that I am the scientist, and that I explained the Lyme crymes to Pam Weintraub (in person, too), yet she claims to have made these assimilations of data independent of myself, by omission, and now via these false threats against my team members.

"Astute Clinician" (Steere) to lecture at NIH - 3 Nov 1999  ◄ You will notice that this was 1999, when I talked to Dr. Dennis Parenti, who informed me about the VAERS or the FDA's Vaccine Adverse Events Reporting System, that led to the FDA's Jan, 2001 hearing on LYMErix, wherein I informed the FDA about what happened with the diagnostic standard, and that no one who attended the Dearborn conference agreed with Allen Steere (meaning it was not a consensus conference).

Pam Weintraub was not in the picture in 1999, with the founding of ActionLyme, and Lyme.org's Karen Forschner has (on Sue Vogan's radio show) and will confirm my version of the series of events.

There is not going to be any Qui Tam award, because we have no Department of Justice.  Pam can relax.  She is not going to become a millionaire whistleblower.  No one is going to become a millionaire whistleblower.  Americans simply do not care about other Americans, as is demonstrated by Pam Weintraub's and Pat Smith's falsehoods to advance themselves and not to benefit the victims of Lyme... who suffer relentlessly.

Everything you see here on ActionLyme, is, in fact, the STUPIDITY that is the result of such arrogance.

THAT'S AMERICA.

If all of the above was not true, the two of them would come forward and admit their crimes.
If all of the above was not true, the AMA would admit to their incompetence.
If all of the above was not true, ALDF/IDSA would admit that they're defending the false status quo because of their previous crimes of blowing off the victims of OspA vaccination with their "guidelines," in addition to changing the diagnostic standard to falsely qualify OspA vaccines and deny the existence of the immune suppression or New Great Imitator versions of Lyme and OspA (and other shed surface antigens) in the first place.
If all of the above was not true Lawrence Altman of the New York Times would admit he, as a CDC officer, is involved in covering up the crimes of other the CDC officers, Alan Barbour and Allen Steere...

Do you see how cowardly they all are?

THAT'S AMERICA.

Land of Greed and Home for Cowards.

Damnation results from putting yourself above the truth.
 
This is the same arrogance (cowardice), the same fear of being less-than another, that sent Lucifer to hell.

 

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CFR Globali$ation  / New World Order ("privileged human beings")

The principles of Eisenstein's relativity are too well known today to require explanation. The humblest reader of this book can undoubtedly give a clear and concise account of such relativistic phenomena as the Michealson-Morley experiment, the Lorentz-Fitzgerald contraction and the Dow-Jones Average. The familiar World-Line Diagram (below) sums it all up.

These are among the results of the same self-aggrandizement (vanity, arrogance, envy, selfishness), Stupidity:

"Diagnosis: Greed" (NYT Judith Warner)

Black Welfare Queen- DHHS Sec Tommy Thompson

Black "Welfare Queens" and the Racially Inferior - NYT Bob Herbert (LOL, Saturday, 11 Oct)

The Banksters are Communists- Noam Chomsky

Crime, Injured People, and Awards- an open letter to Pam Weintraub (greed, outright lies, theft, self-aggrandizement)
 

 

 

 

"Apostasy in the Church (homosexuality or psychiatry) brought in by Vatican II."
"If you are a liar, a perjurer, you are working for Satan."
http://www.postpositive.org/audio/MartinTemptersHour1of3.mp3 ◄ Fr. Malachi Martin,
"The only person who can expel Satan from the Vatican is the Pope."--
"Dr. Hammond [in Hostage to the Devil], the psychiatrist, quit psychiatry and became a Catholic.  'Was Jewish originally."
"Traditional Catholics will be hunted like doves."
"If all religions are true, there are no true religions; there's no such thing as the one true Church,." - meant to be a distraction, cause confusion.
"You only get sanctifying grace through the sacraments."
"New World Order = No country can survive unless they share in the global financial system."
 

http://www.postpositive.org/audio/MartinTemptersHour2of3.mp3  "US is a Marxist state."  "Government control of the masses is Marxism." 
"Where is the militancy?...  that spirit has died out" (not here, on ActionLyme, of course).
"We need to have missions to ourselves."
"Church thoroughly invaded by Masonry."
"Salvation is going to come from the east (Russia, Moscow, Kiev)."
"The biggest role the Anglo-Saxons have been the creators of the Lodge (Masons).  The Lodge is something in which hides the true enemies of the Church.  The Anglo-Saxons (Masons) are the antipathy against the Roman Catholic Church."

"200 NSSM" = "Strategic Necessity" (Kissinger/Bush/Rockefeller).  "Every organization on the US government must contribute to population control."  300 million babies are killed every year around the world.  "Satisfies the Devil's desire to kill off human beings without baptism." 

http://www.postpositive.org/audio/MartinTemptersHour3of3.mp3
"62% of all Catholic couples after two children have undergone sterilization."
"It behooves us Catholics that we undergo persecution just like Christ."  "It behooves the Church to be humiliated."
"The terrible thing is that while Mary watched the torture of her son, she had to WILL it, because that was God's will."
"The characteristic of all crucifixions is sanguis (blood)."
"What happens in the skies ... Our Lady's sign.  It's going to alert everybody.  It will show everybody where they are in God's sight."

 

http://www.youtube.com/watch?v=V-fJ4eNJwQQ&feature=user ◄ "Laws determining the rights of Americans will be determined by non-Americans" (Israelis; PATRIOT Act, "War on Terror," US Army protecting the criminals in the White House, the US-European banking houses determining what's going to happen to our debt,...)
"Create a paradise on earth for the elite." (The Welds, Nancy Johnson (R-New Britain, CT) and her $17,000 free vacation - "The Nature Conservancy" trip to the Easter Islands - then turned over the new Medicare changes to BigPharma)
1957 European economic community visits Pius XIII- "They will have their day, but it will only be a day."

 

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Pam3Cys Immune Suppression = New Great Imitator & LYMErix Diseases
 

"High-Passage G39/40" and Pam3Cys Weintraub (◄Divide and Conquer, the Pat Smith monkey wrench.  Pat Smith of the lymediseaseassociation.org is all about disrupting activism and trashing activists.  If there was no Lyme problem, Pat Smith could not be the Queen of it.  Such a sociopath was the perfect pick by the bad guys to prevent a united activism front.  You can see how dangerous it was having Pat Smith around, trashing Dr. Sam Donta to CT AG Blumenthal, when Dr. Donta was so central to prosecuting the crime.)

Apparently this Pam3Cys immune-suppression information has really shaken up the medical community  (081006 ◄MD speaks out about Yale's abuse of him).   And it is not in Pam Weintraub's book ("Cure Unknown").  This explains Weintraub going off the deep end and threatening my Camp C (for Comprehensive Science) team mates, recently, for making TRUE statements about who wrote the first "Conflicts of Interest" complaint for the State of New York.

Everyone knows I solved the Dearborn testing scam crime (see CRYME DISEASE and the "ROC" nonsense, below by Allen Steere in Europe), since I am the only chemist on any of the teams.  I mean, it's not like I work in a Lyme chemistry lab, I simply, as a scientist, synthesized the data and looked at the Lyme crooks' lab shenanigans (like the Primers Shell Game), since, well, I'm a "dangerously intelligent" chemist, according to Yale University and the State of Corrupticut.  (Camp C is laughing our you-know-whats off.) 
 

http://groups.google.com/groups/search?q=Pam3Cys+Kathleen&start=0&scoring=d&hl=en&  (All)

It's not like Pam Weintraub did not have plenty of years to review my posts to the groups ◄ That was published in 2005. 

B) Here is Pam3Cys, which is what is unique about OspA (LymeRIX):
Immune suppression/dysregulation.
 

Inasmuch as in some people this type of lipoprotein is inflammatory, in
others, it basically shuts off the immune system response to it (we
become tolerized to it).
 

C)  Here is Corixa and SmithKline now joined as one company, creating
allergy vaccines based on what they learned about OspA, represented in
*fungal* antigens like pam3cys/OspA/mycobacterial lipopeptides.:
http://www.corixa.com/default.asp?pid=products
 

THAT IS, people with chronic Lyme, or post-LymeRIX syndrome are immune
suppressed, particularly as regards mycoplasmal and mycobacterial
infections, but also as regards all infections, because as you can see,
Yale is also now interested in the damage they have done activating
Epstein-Barr:
 

http://www.google.com/search?hl=en&q=Yale+and+epstein-Barr+fikrig&btn...
 

'Which was what Paul Duray noted in 1992 about how lymphocytes of
chronic Lyme patients looked, as explained by Duray in Steve Schutzer's
1992 book, "Lyme disease, Molecular and Immunological Approaches."

 

The whole thing is hilarious.  The people who intended to capitalize off of this disease rather than do anything to HELP people, ended up in the moral and social gutter.  You would think a journalist who specializes in science writing would know something about integrity. 

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The bad guys (IDSA/ALDF) actually can't believe they effed up as badly as they did with LYMErix or OspA (Pam3Cys) vaccination.  Their current hysteria (and "guidelines") is meant to be a cover-up of their lies about Lyme and LYMErix.  They're just pretending they don't know Lyme is an immune suppression/opportunistic infection disease like AIDS, and that LYMErix vaccination produces the same outcome.

Read all the reports and related reports:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=Pam3Cys[All+Fields]
 

None of this stuff is in Pam Weintraub's book, "Cure Unknown," by the way, because I hadn't published it by the time her book went to print.  The Pat Smith kooky lymediseaseassociation.org AND the IDSociety.org are hysterical over this at the present time, because it is huge and is the crux of the indictment.  All of the lies about Lyme are about Pam3Cys or OspA.  The Lyme crooks were going to make OspA-hypersensitivity the "disease," and they did that at Dearborn.

No one in Lyme land has to worry about whether they'll be rich and famous whistleblowers or even if they'll be facing jail for homicide, since there's no USDOJ and the country will collapse into chaos very soon.  The reason for the chastisement is the likes of what happened with Lyme - the lack of charity and honesty.  The United States will well-deserve what it gets, as a people.  (I think it's funny because I have witnessed so many vain, arrogant pin-heads running around lying their faces off and blowing their own horns, when they knew nothing, did nothing, and deserved no admiration.)
 

I have not read Pam Weintraub's book, but I know for certain this is not in it because I had not published it yet ("receiver operating characteristic" is not a criterion in validating a method).  This is from the Dearborn booklet, the Dressler/Steere report, where Steere tries to falsely claim that a high concentration of antibodies make the diagnosis more valid:

See CRYMEDISEASE_CHP3_B.htm for an expansion of exactly what Allen Steere did in Europe that is deliberate research fraud and compare to the FDA's rules for the validation of an analytical method.  You can see that there is no such thing as saying that "to detect the highest concentration of an analyte makes it more valid" or "receiver operating characteristic."  In real science, we strive to detect the lowest quantities of anything, reliably.

What Allen Steere did in Europe with the bogus "high passage" strains and this craziness about "receiver operating characteristic" is the crux of the crime- creating the false CDC Dearborn diagnostic standard which only detects late Lyme arthritis in a knee (high antibody concentration, as I explained to the US Attorney, in 2003).

FDA RULES ► http://www.fda.gov/CDER/GUIDANCE/4252fnl.htm 

Specificity and Sensitivity are separate criteria and not to be crossed like this.  This is the bogus "elephant rule" where Steere et al claim that no elephants can be diagnosed as elephants unless they weigh 7 tons or more.  We sure would not want Steere in any biodefense work, or half the nation would be dead from a swine flu pandemic, and Steere would say, "Hey, maybe it's an outbreak of a disease.  I think I will call it the Sneezing Disease." 


FALSE CLAIMS ACT ► http://www.usdoj.gov/usao/eousa/foia_reading_room/usam/title9/crm00921.htm

All the people who make false claims - not just the Lyme crooks - who do not publicly repent and make restitution, are going to hell.  It is a capital sin to bear false witness.  And this includes frauds of omission, or only telling part of the story.  It is especially bad when one lies under oath, especially if the perjurer is a critic of no merit.

 

"The executioners did not allow him to rest long, but bade him rise and place himself on the cross that they might nail him to it. Then seizing his right arm they dragged it to the hole prepared for the nail, and having tied it tightly down with a cord, one of them knelt upon his sacred chest, a second held his hand flat, and a third taking a long thick nail, pressed it on the open palm of that adorable hand, which had ever been open to bestow blessings and favours on the ungrateful Jews, and with a great iron hammer drove it through the flesh, and far into the wood of the cross. Our Lord uttered one deep but suppressed groan, and his blood gushed forth and sprinkled the arms of the archers. I counted the blows of the hammer, but my extreme grief made me forget their number. The nails were very large, the heads about the size of a crown piece, and the thickness that of a man’s thumb, while the points came through at the back of the cross. The Blessed Virgin stood motionless; from time to time you might distinguish her plaintive moans; she appeared as if almost fainting from grief, and Magdalen was quite beside herself. When the executioners had nailed the right hand of our Lord, they perceived that his left hand did not reach the hole they had bored to receive the nail, therefore they tied ropes to his left arm, and having steadied their feet against the cross, pulled the left hand violently until it reached the place prepared for it. This dreadful process caused our Lord indescribable agony, his breast heaved, and his legs were quite contracted. They again knelt upon him, tied down his arms, and drove the second nail into his left hand; his blood flowed afresh, and his feeble groans were once more heard between the blows of the hammer, but nothing could move the hard-hearted executioners to the slightest pity. The arms of Jesus, thus unnaturally stretched out, no longer covered the arms of the cross, which were sloped; there was a wide space between them and his armpits. Each additional torture and insult inflicted on our Lord caused a fresh pang in the heart of his Blessed Mother; she became white as a corpse, but as the Pharisees endeavoured to increase her pain by insulting words and gestures, the disciples led her to a group of pious women who were standing a little farther off....

http://www.jesus-passion.com/THE_PASSION_3.5.htm#CHAPTER%20XXXVIII

 

This is the savagery one can expect in return for giving people the truth.  I recommend that everyone  should read the whole thing, because the people who crucified Him were jealous that Christ might steal their thunder.  Salvation is so simple.  Never put yourself above the truth. 

 

========================================

 

BLEBBING or the shedding of Pam3Cys and other surface antigens is like autovaccination or begins the autotolerization process:

"He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. "It's using some sort of stealth-bomber-type mechanism," he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: "It's like a bacterial Star Wars defense program," in which released surface proteins might intercept incoming host antibodies keeping the spirochetes safe from immunological attack."
-- 1996, Alan Barbour et al; The CDC Crooks.

 

And it's not like they didn't know:

Gary Wormser reporting the blunting of the immune response in OspA vaccinated animals:
http://www.ncbi.nlm.nih.gov/pubmed/10865170?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

"OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression."

 

It's possible that the crooks don't want us treated for Lyme because we might create more antibiotic resistant tuberculosis and the like, since fungal antigens, as found in Lyme and tuberculosis, create a condition of immune incompetence to similar antigens (tuberculosis).

Toll-like receptor 2 downregulation in established mouse allergic lungs contributes to decreased mycoplasma clearance

 

10) Leishmania donovani infection down-regulates TLR2-stimulated IL-12p40 and activates IL-10 in cells of macrophage/monocytic lineage by modulating MAPK pathways through a contact-dependent mechanism.

http://www.ncbi.nlm.nih.gov/pubmed/18778366?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Chandra D, Naik S.

Department of Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow, India.

The failure of Leishmania, an intracellular pathogen, to stimulate a pro-inflammatory response following entry into macrophages has been well reported. This occurs in spite of the fact that ligands for the toll-like receptors (TLR) have been recently shown on the parasite surface and their role in disease protection well documented. The outcome of infection in leishmaniasis is determined by the Th1 versus Th2 nature of the effector response and the generation of IL-12 and IL-10 by the infected macrophages is important for this decision. We evaluated the effect of L. donovani infection of monocytes (cell line THP-1, and monocytes derived from human peripheral blood) on Pam3cys (TLR2 ligand) and lipopolysaccharide (TLR4 ligand) stimulated production of IL-12p40 and IL-10. L. donovani infection caused suppression of TLR2 and TLR4-stimulated IL-12p40, with an increase in IL-10 production. Parasites also modulated the TLR2-stimulated mitogen-activated protein kinase (MAPK) pathway by suppressing MAPK P(38) phosphorylation and activating extracellular regulated kinase (ERK)1/2 phosphorylation. These effects could be reversed either by using a MAPK P(38) activator, anisomycin, or ERK1/2 inhibitor, U0126. L. donovani caused modulation of TLR2-stimulated MAPK pathways in a contact-dependent mechanism. In addition parasite structural integrity but not viability was required for suppression of TLR2-stimulated IL-12p40 and activation of IL-10. These observations suggest that L. donovani has evolved survival strategies that subvert the pro-inflammatory response generated through TLRs.

 

9) BRUCELLA and Pam3Cys causing immune suppression:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17984211

Copyright © 2008, American Society for Microbiology
 

Brucella abortus Inhibits Major Histocompatibility Complex Class II Expression and Antigen Processing through Interleukin-6 Secretion via Toll-Like Receptor 2

Infect Immun. 2008 January; 76(1): 250–262.

The strategies that allow Brucella abortus to survive inside macrophages for prolonged periods and to avoid the immunological surveillance of major histocompatibility complex class II (MHC-II)-restricted gamma interferon (IFN-γ)-producing CD4⁺ T lymphocytes are poorly understood. We report here that infection of THP-1 cells with B. abortus inhibited expression of MHC-II molecules and antigen (Ag) processing. Heat-killed B. abortus (HKBA) also induced both these phenomena, indicating the independence of bacterial viability and involvement of a structural component of the bacterium. Accordingly, outer membrane protein 19 (Omp19), a prototypical B. abortus lipoprotein, inhibited both MHC-II expression and Ag processing to the same extent as HKBA. Moreover, a synthetic lipohexapeptide that mimics the structure of the protein lipid moiety also inhibited MHC-II expression, indicating that any Brucella lipoprotein could down-modulate MHC-II expression and Ag processing. Inhibition of MHC-II expression and Ag processing by either HKBA or lipidated Omp19 (L-Omp19) depended on Toll-like receptor 2 and was mediated by interleukin-6. HKBA or L-Omp19 also inhibited MHC-II expression and Ag processing of human monocytes. In addition, exposure to the synthetic lipohexapeptide inhibited Ag-specific T-cell proliferation and IFN-γ production of peripheral blood mononuclear cells from Brucella-infected patients. Together, these results indicate that there is a mechanism by which B. abortus may prevent recognition by T cells to evade host immunity and establish a chronic infection.

From the 1989 IDSA Reviews Special Supplement on Lyme and Spirochetal Diseases, article by Paul Duray:

Mycoplasma fermentans infection promotes immortalization of human peripheral blood mononuclear cells in culture.
http://www.ncbi.nlm.nih.gov/pubmed/15331449?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Blood. 2004 Dec 15;104(13):4252-9. Epub 2004 Aug 26.
 

Department of Infectious and Parasitic Diseases Pathology, American Registry of Pathology, Washington DC, USA.

Chronic infection or colonization by mycoplasma(s) could gradually and significantly alter many biologic properties of mammalian host cells in culture, including induction of malignant transformation. We examined effects of Mycoplasma fermentans infection on the continuing survival and immortality of human peripheral blood mononuclear cells (PBMCs) from healthy blood donors. Without specific supplemental growth factors, human PBMCs normally die rapidly, with few cells other than macrophages/monocytes surviving after 2 weeks in cultures. Only occasional Epstein-Barr virus (EBV)-positive B lymphocytes would continue to proliferate and undergo spontaneous immortalization. Our present study revealed that infection of human PBMCs in culture with the incognitus and PG18 strains of M fermentans, but surprisingly not with some other strains tested in parallel, markedly enhanced the rate of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%). Compared with spontaneously immortalized PBMCs, the PBMCs immortalized in cultures infected with the mycoplasmas often had prominent karyotype changes with chromosomal loss, gain, or translocations. Furthermore, many of these immortalized B lymphocytes were found to be monoclonal in nature. The in vitro findings would be of relevance to lymphoproliferative disorders that occurred in patients with immune suppression. The mycoplasma-mediated promotional effect in cell immortalization and its potential clinical implications warrant further study.

THE MECHANICS OF FUNGAL-ANTIGEN-RELATED IMMUNE SUPPRESSION-  Brought to you as a summary of the available science.   Were there any responsible MDs who dared to pass up the Yale Lyme Kool-Aid and do their homework, you would not be reading it all here, first.

 

1) Tolerance Induced by the Lipopeptide Pam₃Cys [OspA] Is Due to Ablation of IL-1R-Associated Kinase-1¹  

"Although a single ligation of TLRs induces responses such as TNF production, repeated ligation will lead to a loss of response, i.e., the cells become tolerant."   http://www.jimmunol.org/cgi/content/full/173/4/2736

 

2) "Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression" - 

"In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12819085

 

3) Mycobacterium tuberculosis LprG (Rv1411c): A Novel TLR-2 Ligand That Inhibits Human Macrophage Class II MHC Antigen Processing¹
 http://www.jimmunol.org/cgi/content/full/173/4/2660    

The Journal of Immunology, 2004, 173: 2660-2668.
Copyright © 2004 by The American Association of Immunologists
 

 "Signaling through TLR-2 by lipoproteins may represent a double-edged sword for host responses to chronic intracellular pathogens such as M. tuberculosis. Short-term signaling through TLR-2 activates macrophages and initiates acute inflammation that may help control initial infection. In contrast, prolonged TLR-2 signaling in macrophages results in down-regulation of certain critical immune functions, such as MHC-II Ag processing. M. tuberculosis infects, survives, and persists in macrophages. The ability of M. tuberculosis to survive acute inflammation positions the bacilli to take advantage, through secretion of lipoproteins such as LprG and LpqH, of this down-regulation of macrophage immune function." 
 

4) Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates Innate Immune Responses¹
http://www.jimmunol.org/cgi/content/full/173/4/2683
 

"Lipoproteins and lipopeptides have been identified in a large number of microorganisms, the most prominent ones being mycobacteria, mycoplasms, and spirochetes. They have been found to exhibit both a strong innate inflammatory response in the host and an enduring adaptive immune response in mammalian hosts (16). The strong proinflammatory capacities of lipoproteins were first described for outer surface proteins A and B of Borrelia burgdorferi, which are also highly immunogenic (17) and have lately been the basis for a Lyme disease vaccine development (18). These compounds exhibit an triacylated lipid anchor structure comprising an N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2RS)-propyl]-(R)-cysteinyl (Pam₃Cys) moiety at the N terminus (19), a feature that was previously described for the Braun lipoprotein from Escherichia coli (20). Because the N-terminal Pam₃Cys modification is essential for immunoactivation caused by lipoproteins of B. burgdorferi as well as of another spirochete, Treponema pallidum (21), subsequent studies investigating immune responses to spirochetes used synthetic lipopeptides (22). The Pam₃Cys moiety was also reported to be present in cytokine-inducing lipoproteins of Mycobacterium and Mycoplasma spp. (23, 24); thus, it can be regarded as a highly conserved molecular motif among different classes of bacteria. In Mycoplasma fermentans, the presence of a macrophage stimulating lipopeptide, termed 2-kDa macrophage-activating lipopeptide (MALP-2), was observed, being stimulatory active at picomolar concentrations (25). This compound, in contrast to the predominant lipopeptide structures present in lipoproteins of E. coli, B. burgdorferi, and mycobacteria, lacks the N-palmitoyl group, thus containing a diacylated (Pam₂Cys) lipid anchor structure at the N terminus. Following studies revealed the presence of closely related compounds in other Mycoplasma spp. (26).."   
 

"Toll-like receptors (TLRs) 2 and 4 are signal transducers for lipopolysaccharide, the major proinflammatory constituent in the outer membrane of Gram-negative bacteria. We observed that membrane lipoproteins/lipopeptides from Borrelia burgdorferi, Treponema pallidum, and Mycoplasma fermentans activated cells heterologously expressing TLR2 but not those expressing TLR1 or TLR4. These TLR2-expressing cells were also stimulated by living motile B. burgdorferi, suggesting that TLR2 recognition of lipoproteins is relevant to natural Borrelia infection. Importantly, a TLR2 antibody inhibited bacterial lipoprotein/lipopeptide-induced tumor necrosis factor release from human peripheral blood mononuclear cells, and TLR2-null Chinese hamster macrophages were insensitive to lipoprotein/lipopeptide challenge. The data suggest a role for the native protein in cellular activation by these ligands. In addition, TLR2-dependent responses were seen using whole Mycobacterium avium and Staphylococcus aureus, demonstrating that this receptor can function as a signal transducer for a wide spectrum of bacterial products. We conclude that diverse pathogens activate cells through TLR2 and propose that this molecule is a central pattern recognition receptor in host immune responses to microbial invasion."   http://www.jimmunol.org/cgi/content/full/173/4/2683

 

5) http://www.jleukbio.org/cgi/content/full/75/3/460

It is interesting that in this Tg mouse model, antigen-presenting cells (macrophages and dendritic and B cells) rather than T cells provide the major source of elevated HIV-1 production. Furthermore, we have recently demonstrated that known TLR agonists such as LPS, monosylated phosphatidylinositol, CpG, and S-[2,3-bis(palmitoyloxy)-(2-RS)-propyl]-N-palmitoyl-(R)-Cys-(S)-Ser-Lys4-OH, trihydrochloride (Pam3Cys) stimulate increased levels of HIV-1 transcripts as well as production of p24 (a capsid protein encoded by the gag gene) by Tg spleen cells in vitro [¹⁵ , ¹⁶ ].

In the present report, we show that after tolerization with TLR2, TLR4, or TLR9 ligands, Tg cells unexpectedly display enhanced HIV-1 gene and protein expression after restimulation in vitro despite dramatic reductions in proinflammatory cytokine production. Moreover, Tg mice tolerized in vivo with LPS or Pam3Cys show increased levels of plasma p24, whereas TNF- production is markedly diminished in the same animals. This overexpression of HIV-1 genes following TLR reprogramming may reflect a mechanism used by the virus to escape the effects of microbial-induced tolerance during natural infection in vivo.

 

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

Báfica A, Scanga CA, Equils O, Sher A.

Immunobiology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA. abafica@niaid.nih.gov

Microbial-induced proinflammatory pathways are thought to play a key role in the activation of human immunodeficiency virus type 1 (HIV-1) gene expression. The induction of Toll-like receptor (TLR) tolerance leads to a complex reprogramming in the pattern of inflammatory gene expression and down-modulates tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1, and IL-6 production. Using transgenic (Tg) mice that incorporate the entire HIV-1 genome, including the long-terminal repeat, we have previously demonstrated that a number of different TLR ligands induce HIV-1 gene expression in cultured splenocytes as well as purified antigen-presenting cell populations. Here, we have used this model to determine the effect of TLR-mediated tolerance as an approach to inhibiting microbial-induced viral gene expression in vivo. Unexpectedly, Tg splenocytes and macrophages, rendered tolerant in vitro to TLR2, TLR4, and TLR9 ligands as assessed by proinflammatory cytokine secretion and nuclear factor-kappaB activation, showed enhanced HIV-1 p24 production. A similar enhancement was observed in splenocytes tolerized and then challenged with heterologous TLR ligands. Moreover, TLR2- and TLR4-homotolerized mice demonstrated significantly increased plasma p24 production in vivo despite lower levels of TNF-alpha. Together, these results demonstrate that HIV-1 expression is enhanced in TLR-reprogrammed host cells, possibly reflecting a mechanism used by the virus to escape the effects of microbial-induced tolerance during natural infection in vivo.

 

See?  That's a major F-up, that might have been investigated sooner, had the Yale Lyme crooks told the truth about LYMErix in the mid-1990s when they were having their fake OspA (Pam3Cys) trials, for which the changed the diagnostic standard for Lyme.  This is in addition to the fact that OspA was never shown to prevent Lyme in lab animals.

That's 5 reports that showed OspA failed in animals, 3 reports that showed fungal antigens failed in tuberculosis vaccines, plus the 8 reports you see here.

 

6) AUGUST, 2008:

Human immunodeficiency virus infection alters tumor necrosis factor alpha production via Toll-like receptor-dependent pathways in alveolar macrophages and U1 cells.
http://www.ncbi.nlm.nih.gov/pubmed/18524817?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Nicol MQ, Mathys JM, Pereira A, Ollington K, Ieong MH, Skolnik PR.

Center for HIV/AIDS Care and Research, Boston University School of Medicine, Boston, MA 02118-2393, USA. mnicol@bu.edu

Human immunodeficiency virus (HIV)-positive persons are predisposed to pulmonary infections, even after receiving effective highly active antiretroviral therapy. The reasons for this are unclear but may involve changes in innate immune function. HIV type 1 infection of macrophages impairs effector functions, including cytokine production. We observed decreased constitutive tumor necrosis factor alpha (TNF-alpha) concentrations and increased soluble tumor necrosis factor receptor type II (sTNFRII) in bronchoalveolar lavage fluid samples from HIV-positive subjects compared to healthy controls. Moreover, net proinflammatory TNF-alpha activity, as measured by the TNF-alpha/sTNFRII ratio, decreased as HIV-related disease progressed, as manifested by decreasing CD4 cell count and increasing HIV RNA (viral load). Since TNF-alpha is an important component of the innate immune system and is produced upon activation of Toll-like receptor (TLR) pathways, we hypothesized that the mechanism associated with deficient TNF-alpha production in the lung involved altered TLR expression or a deficit in the TLR signaling cascade. We found decreased Toll-like receptor 1 (TLR1) and TLR4 surface expression in HIV-infected U1 monocytic cells compared to the uninfected parental U937 cell line and decreased TLR message in alveolar macrophages (AMs) from HIV-positive subjects. In addition, stimulation with TLR1/2 ligand (Pam(3)Cys) or TLR4 ligand (lipopolysaccharide) resulted in decreased intracellular phosphorylated extracellular signal-regulated kinase and subsequent decreased transcription and expression of TNF-alpha in U1 cells compared to U937 cells. AMs from HIV-positive subjects also showed decreased TNF-alpha production in response to these TLR2 and TLR4 ligands. We postulate that HIV infection alters expression of TLRs with subsequent changes in mitogen-activated protein kinase signaling and cytokine production that ultimately leads to deficiencies of innate immune responses that predispose HIV-positive subjects to infection.

 

7) http://www.jimmunol.org/cgi/content/full/170/1/508

Prior exposure to LPS both in vitro and in vivo can lead to desensitization of immune cells to subsequent challenge with LPS, a phenomenon that has been referred to as "endotoxin tolerance."

Induction of in vitro reprogramming by Toll-like receptor (TLR)2 and TLR4 agonists in murine macrophages: effects of TLR "homotolerance" versus "heterotolerance" on NF-kappa B signaling pathway components.

Dobrovolskaia MA, Medvedev AE, Thomas KE, Cuesta N, Toshchakov V, Ren T, Cody MJ, Michalek SM, Rice NR, Vogel SN.

Department of Microbiology and Immunology, University of Maryland, Baltimore, MD 21201, USA.

In this study, tolerance induction by preexposure of murine macrophages to Toll-like receptor (TLR)2 and TLR4 agonists was revisited, focusing on the major signaling components associated with NF-kappaB activation. Pretreatment of macrophages with a pure TLR4 agonist (protein-free Escherichia coli (Ec) LPS) or with TLR2 agonists (Porphyromonas gingivalis LPS or synthetic lipoprotein Pam3Cys) led to suppression of TNF-alpha secretion, IL-1R-associated kinase-1, and IkappaB kinase (IKK) kinase activities, c-jun N-terminal kinase, and extracellular signal-regulated kinase phosphorylation, and to suppression of NF-kappaB DNA binding and transactivation upon challenge with the same agonist (TLR4 or TLR2 "homotolerance," respectively). Despite inhibited NF-kappaB DNA binding, increased levels of nuclear NF-kappaB were detected in agonist-pretreated macrophages. For all the intermediate signaling elements, heterotolerance was weaker than TLR4 or TLR2 homotolerance with the exception of IKK kinase activity. IKK kinase activity was unperturbed in heterotolerance. TNF-alpha secretion was also suppressed in P. gingivalis LPS-pretreated, Ec LPS-challenged cells, but not vice versa, while Pam3Cys and Ec LPS did not induce a state of cross-tolerance at the level of TNF-alpha. Experiments designed to elucidate novel mechanisms of NF-kappaB inhibition in tolerized cells revealed the potential contribution of IkappaBepsilon and IkappaBxi inhibitory proteins and the necessity of TLR4 engagement for induction of tolerance to Toll receptor-IL-1R domain-containing adapter protein/MyD88-adapter-like-dependent gene expression. Collectively, these data demonstrate that induction of homotolerance affects a broader spectrum of signaling components than in heterotolerance, with selective modulation of specific elements within the NF-kappaB signaling pathway.

 

 

8)  Lipid-associated membrane proteins of Mycoplasma fermentans and M. penetrans activate human immunodeficiency virus long-terminal repeats through Toll-like receptors

Takashi Shimizu, Yutaka Kida, and Koichi Kuwano

Department of Bacteriology, Kurume University School of Medicine, Kurume, Japan

 

Immunology. 2004 September; 113(1): 121–129.

doi: 10.1111/j.1365-2567.2004.01937.x.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15312143
 

Mycoplasmas are known to enhance human immunodeficiency virus (HIV) replication, and mycoplasma-derived lipid extracts have been reported to activate nuclear factor-κB (NF-κB) through Toll-like receptors (TLRs). In this study, we examined the involvement of TLRs in the activation of HIV long-terminal repeats (LTR) by mycoplasma and their active components responsible for the TLR activation. Lipid-associated membrane proteins (LAMPs) from two species of mycoplasma (Mycoplasma fermentans and M. penetrans) that are associated with acquired immune-deficiency syndrome (AIDS), were found to activate HIV LTRs in a human monocytic cell line, THP-1. NF-κB deletion from the LTR resulted in inhibition of the activation. The LTR activation by M. fermentans LAMPs was inhibited by a dominant negative (DN) construct of TLR1 and TLR6, whereas HIV LTR activation by M. penetrans LAMPs was inhibited by DN TLR1, but not by DN TLR6. These results indicate that the activation of HIV LTRs by M. fermentans and M. penetrans LAMPs is dependent on NF-κB, and that the activation of HIV LTR by M. fermentans LAMPs is mediated through TLR1, TLR2 and TLR6. In contrast, the LTR activation by M. penetrans LAMPs is carried out through TLR1 and TLR2, but not TLR6. Subsequently, the active component of M. penetrans and M. fermentans LAMPs was purified by reverse-phase high-performance liquid chromatography (HPLC). Interestingly, the purified lipoprotein of M. penetrans LAMPs (LPMp) was able to activate NF-κB through TLR1 and TLR2. On the other hand, the activation of NF-κB by purified lipoprotein of M. fermentans LAMPs (LPMf) was mediated through TLR2 and TLR6, but not TLR1.

Keywords: HIV, lipoprotein, mycoplasma, Toll-like receptor

 

In mycoplasmas, acylated proteins are abundant cell-surface antigens, and many putative lipoprotein-encoding genes have been identified in the sequenced mycoplasma genomes.^49,50 It is, at present, controversial as to whether or not mycoplasmas have triacylated lipoprotein. Chemically identified lipoproteins from M. fermentans,⁴⁴M. hyorhinis,⁵¹M. salivarium⁴⁶ and M. gallisepticum⁵² are not N-acylated, nor has an N-acyltransferase gene been found in M. pneumoniae,⁵³M. genitalium⁵⁴ or M. penetrans⁵⁵ genomes. To date, the presence of proteins with N-acyltransferase activity has not been clearly established. However, the study on the ratio of N-amide and O-ester bonds in M. gallisepticum and M. mycoides may indicate the presence of diacylated and triacylated lipoproteins.⁵⁶ The resistance to Edoman degradation of proteins from M. mycoides also indicates the presence of N-acylation.⁵⁰ In this study, we found that the lipoprotein separated from M. penetrans induced NF-κB through TLR1 and TLR2. Triacylated lipoproteins, such as Pam3-CSK4, have been reported to be recognized by TLR1 and TLR2,⁴³ whereas diacylated lipoproteins, such as MALP-2, have been shown to be recognized by TLR2 and TLR6.⁴² Interestingly, synthetically triacylated MALP-2, N-palamitoyl-MALP-2, was not recognized by TLR6.⁵⁷ These findings may indicate the existence of triacylated lipoproteins in mycoplasma species.

 

 

9) BRUCELLA and Pam3Cys causing immune suppression:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17984211

Copyright © 2008, American Society for Microbiology

Brucella abortus Inhibits Major Histocompatibility Complex Class II Expression and Antigen Processing through Interleukin-6 Secretion via Toll-Like Receptor 2

Infect Immun. 2008 January; 76(1): 250–262.

The strategies that allow Brucella abortus to survive inside macrophages for prolonged periods and to avoid the immunological surveillance of major histocompatibility complex class II (MHC-II)-restricted gamma interferon (IFN-γ)-producing CD4⁺ T lymphocytes are poorly understood. We report here that infection of THP-1 cells with B. abortus inhibited expression of MHC-II molecules and antigen (Ag) processing. Heat-killed B. abortus (HKBA) also induced both these phenomena, indicating the independence of bacterial viability and involvement of a structural component of the bacterium. Accordingly, outer membrane protein 19 (Omp19), a prototypical B. abortus lipoprotein, inhibited both MHC-II expression and Ag processing to the same extent as HKBA. Moreover, a synthetic lipohexapeptide that mimics the structure of the protein lipid moiety also inhibited MHC-II expression, indicating that any Brucella lipoprotein could down-modulate MHC-II expression and Ag processing. Inhibition of MHC-II expression and Ag processing by either HKBA or lipidated Omp19 (L-Omp19) depended on Toll-like receptor 2 and was mediated by interleukin-6. HKBA or L-Omp19 also inhibited MHC-II expression and Ag processing of human monocytes. In addition, exposure to the synthetic lipohexapeptide inhibited Ag-specific T-cell proliferation and IFN-γ production of peripheral blood mononuclear cells from Brucella-infected patients. Together, these results indicate that there is a mechanism by which B. abortus may prevent recognition by T cells to evade host immunity and establish a chronic infection.

 

 

TUBERCULOSIS (FUNGAL) VACCINES FAILURES:

Clin Exp Immunol. 2000 May;120(2):274-9.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792376&dopt=Abstract
The 19-kD antigen and protective immunity in a murine model of tuberculosis. 
Yeremeev VV, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J, Young DB.

"The 19-kD antigen is a cell wall-associated lipoprotein present in Mycobacterium tuberculosis and in bacille Calmette-Guérin (BCG) vaccine strains. Expression of the 19-kD antigen as a recombinant protein in two saprophytic mycobacteria-M. vaccae and M. smegmatis-resulted in abrogation of their ability to confer protection against M. tuberculosis in a murine challenge model, and in their ability to prime a DTH response to cross-reactive mycobacterial antigens. Induction of an immune response to the 19-kD antigen by an alternative approach of DNA vaccination had no effect on subsequent M. tuberculosis challenge. These results are consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of vaccination with live mycobacteria. Targeted inactivation of genes encoding selected antigens represents a potential route towards development of improved vaccine candidates."

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract

Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.

Post FA, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
 

Vaccination of mice with Mycobacterium vaccae or M. smegmatis induces some protection against M. tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective immunity. To investigate the mechanism of this suppression of immunity, human monocyte-derived macrophages (MDM) were infected with M. smeg19kDa. Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). Infection with M. smeg19kDa and with M. smegV had no differential effect on expression of costimulatory molecules on MDM, nor did it affect the proliferation of presensitized T cells cocultured with infected MDM. When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. When the purified 19-kDa lipoprotein was added directly to cultures of infected monocytes, there was little effect on either induction of cytokine production or its inhibition. Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation."

 

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093

  Infect Immun. 2003 Jun;71(6):3146-54. Related Articles, Links

  
The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1-type immune response deleterious to protection.

Hovav AH, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A, Bercovier H.

Department of Clinical Microbiology, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.

Th1 immune response is essential in the protection against mycobacterial intracellular pathogens. Lipoproteins trigger both humoral and cellular immune responses and may be candidate protective antigens. We studied in BALB/c mice the immunogenicity and the protection offered by the recombinant 27-kDa Mycobacterium tuberculosis lipoprotein and the corresponding DNA vaccine. Immunization with the 27-kDa antigen resulted in high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical Th1 profile and a strong delayed hypersensitivity response. A strong proliferation response was observed in splenocytes, and significant nitric oxide production and gamma interferon secretion but not interleukin 10 secretion were measured. Based on these criteria, the 27-kDa antigen induced a typical Th1-type immune response thought to be necessary for protection. Surprisingly, in 27-kDa-vaccinated mice (protein or DNA vaccines) challenged by M. tuberculosis H37Rv or BCG strains, there was a significant increase in the numbers of CFU in the spleen compared to that for control groups. Furthermore, the protection provided by BCG or other mycobacterial antigens was completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study indicates that the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines. We are currently studying how the 27-kDa antigen modulates the mouse immune response.

 

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