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» LymeNet Flash » Questions and Discussion » Medical Questions » Hep B provides PROTECTION from lyme - OspC and stationary phase

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Author Topic: Hep B provides PROTECTION from lyme - OspC and stationary phase
Marnie
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Hepatitis B Virus Capsid-like Particles Can Display the Complete,

Dimeric Outer Surface Protein C

and Stimulate Production of

Protective Antibody Responses

against Borrelia burgdorferi Infection

coreOspCa and coreOspCb, efficiently formed

***stable CLPs*** (capsid-like particles)

http://www.jbc.org/content/281/25/17474

Hepatitis B virus induces expression of

antioxidant response element-regulated genes by

***activation of Nrf2.***

The HBV-dependent induction of Nrf2/ARE-regulated genes

might ensure survival of the infected cell, shape the immune response to HBV, and thereby

promote establishment of the infection.

http://www.ncbi.nlm.nih.gov/pubmed/20956535


When Nrf2 is upregulated, iNOS is downregulated.

The nuclear factor erythroid 2–related factor 2 = antioxidant stress response.

iNOS = Inducible nitric oxide synthase -> NO, nitric oxide.

Such appears to be the reaction to berberine i.e., activates Nrf2, inhibits iNOS (and MUCH more) which looks to be beneficial to fight some pathogens (and cancers), but NOT ALL.

We know that Bb has to express OspC when it goes from the tick's gut to us...when it senses "food", but also "danger".

"the downregulation of OspA requires RpoS production"

(Stress response)

elevated rpoS transcription directly
correlated to

increased carotenoid production

http://webcache.googleusercontent.com/search?q=cache:W2NNi_NgJ_oJ:http://homepages.rpi.edu/~koffam/papers/2009_Chemler_Fowler_Koffas.pdf

Carotenoids are organic pigments that are found in the chloroplasts and chromoplasts of plants and some other

photosynthetic organisms, including some bacteria

and some fungi.

Carotenoids can be produced

*from fats* and other basic organic metabolic building blocks

by all these organisms.

All carotenoids are tetraterpenoids, meaning that they are produced from 8 isoprene molecules and contain

40 carbon atoms.

Bb can then store carbon:

***carbon storage regulator A protein (CsrABb)***;

The carbon storage regulator A (CsrA) is a protein responsible for the

repression of

a variety of stationary-phase genes in bacteria.

http://jb.asm.org/content/187/10/3496.abstract

Carbon storage regulator A (CsrABb) is a

repressor of Borrelia burgdorferi flagellin protein FlaB

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2958.2011.07853.x/abstract

Later...flagellin is a big problem:

Both Hsp70 and flagellin were

inaccessible to monoclonal antibodies against them

***when bound to Hsp60.***

In one experiment, investigators treated various mice

***with DOPA***

and discovered significant upregulation of

HSP60 expression in the mitochondria

and HSP70 expression in the cytoplasm."

Hsp70 was found to bind flagellin

at all temperatures tested between 33 and 41 degrees C.

This association could be decreased with ATP when cells had been incubated at 41 degrees C during radioactive labeling but not at lower temperatures.

Both flagellin and Hsp70 were found to

associate with Hsp60,

forming a complex of the three proteins.

Hsp70 association with this complex could be decreased with ATP, but

flagellin binding to Hsp60 was ATP independent at all temperatures studied.

Both Hsp70 and flagellin were

inaccessible to monoclonal antibodies against them

when bound to Hsp60.

These studies suggest that in B. burgdorferi,

a major function of Hsp60 and Hsp70

is in the molecular processing of flagellin."

http://jb.asm.org/content/176/21/6449.abstract

HSP60 plays an important role in the transport and maintenance of mitochondrial proteins as well as the transmission and

replication of mitochondrial DNA.

However, some new research has indicated that HSP60 possibly plays a role in a “danger signal cascade” immune response.

There is also mounting evidence that it plays a role in autoimmune disease.

HSP60 has been shown to be *released from* specific cells like peripheral blood mononuclear cells (PBMCs) when there are lipopolysaccharides (LPS) or GroEL present.

Wiki.

If it is needed for mitochondrial DNA replication, another process has to kick in to make more mitochondria (biogenesis).

In steps the dangerous IL-15:

We have shown here that ***CD8(+) memory T cells***,

but not CD8(+) T effector (Teff) cells,

possessed

substantial mitochondrial spare respiratory capacity (SRC).

SRC is the extra capacity available in cells to produce energy in response to increased stress or work and as such is associated with cellular survival.

We found that interleukin-15 (IL-15), a cytokine critical for CD8(+) memory T cells, regulated SRC and oxidative metabolism

by ***promoting mitochondrial biogenesis***

and expression of carnitine palmitoyl transferase (CPT1a), a metabolic enzyme that controls the rate-limiting step to mitochondrial fatty acid oxidation (FAO).

http://www.ncbi.nlm.nih.gov/pubmed/22206904

Memory T cells are believed to last up to 15 yr in humans

as seen in smallpox immunization, but the mechanism by which this occurs is an open question.

Evidence suggests that signals from the γc cytokines IL-7 and IL-15 are critical in the maintenance of memory CD8 T cells.

http://jem.rupress.org/content/204/3/619.full

Back to Bb's stationary phase...

In addition, during starvation, clpP and, to a somewhat lesser extent, clpA are involved in

maintaining ongoing Dps synthesis (acting at the level of Dps translation),

which is required for

strong Dps accumulation in long-term stationary phase cells.

http://www.ncbi.nlm.nih.gov/pubmed/12950924?dopt=Abstract

Dps = DNA-binding proteins from starved cells

DPS proteins are part of a complex bacterial defense system that protects DNA against oxidative damage and are distributed widely in the bacterial kingdom.

Borrelia Dps forms a dodecameric complex capable of

sequestering iron.

http://www.ncbi.nlm.nih.gov/pubmed/17181780

Bb, it appears, sequesters iron and has a transferrin gene...iron out, so to speak - into biofilm which is where the
Fe is oxidized instead of Bb's proteins.

LuxS mediates *iron-dependent* biofilm formation for “quorum sensing”

http://www.ncbi.nlm.nih.gov/pubmed/12117917


“Degradation of RpoS by ClpXP."

(Stress gone...degrade the RpoS protein.)


"ClpXP must use its maximum successive firing capacity of four subunits to
unfold

***stable substrates*** like GFP."

(Green Fluorescent Protein = GFP)

and the selective expression of

***GFP in the stationary phase***

based on the co-expression of ***GFP and OspC..***

If you are curious, more about GFP here:

http://en.wikipedia.org/wiki/Green_fluorescent_protein

Pay close attention to indole...as it relates to tryptophan...

There are other ways to upregulate Nrf2...

Here are some possibilities:

http://www.ncbi.nlm.nih.gov/pubmed/17219054

http://www.ncbi.nlm.nih.gov/pubmed/22469516

http://www.ncbi.nlm.nih.gov/pubmed/20805228

"Nrf2 is referred to as the “master regulator” of the antioxidant response,

modulating the expression of hundreds of genes, including not only the familiar antioxidant enzymes,

but large numbers of genes that control seemingly disparate processes such as immune and inflammatory responses,

tissue remodeling and fibrosis, carcinogenesis and metastasis, and

even cognitive dysfunction and addictive behavior."

http://www.sciencedirect.com/science/article/pii/S0098299711000501

The ANTI-oxidant ubiquinOL (mitochondria ubiquinone -> ubiquinOL if able) has very recently been found to help those with autism.

There are many genetic problems and.or many infections that trigger "mitochondrial dysfunction" and as we age, the process accelerates.

http://www.iflscience.com/health-and-medicine/anti-aging-formula-slated-begin-human-trials

Bb loves NADH...

that BbCoADR is necessary to maintain optimal redox ratios for

CoA/CoA-disulphide and

NAD(+) /NADH during periods of rapid replication

throughout the enzootic cycle, to support thiol-disulphide homeostasis,

and to indirectly protect the spirochaete against peroxide-mediated membrane damage;

one or more of these functions are essential for infection of the mammalian host by B. burgdorferi.

http://www.ncbi.nlm.nih.gov/pubmed/21923763

Ancora Imparo. I hope this helps those interested in understanding Bb and our response.

COX2, PGE2, miRNA-146a,suppressor macrophages, et al = even longer explanation that the above!

[ 08-16-2014, 03:11 PM: Message edited by: Marnie ]

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Razzle
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So would a Hep B vaccine (does such a thing exist?) also help prevent Lyme transmission from a tick to a human?

--------------------
-Razzle
Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs.

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Marnie
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Might.

Not yet.

One has to "grasp" the dangers of vaccines though in certain persons...genetics IS involved.

If someone is "skewed" towards a Th2 type immune response - genetically - and is given a vaccine destined to require a TH1 antibody response maybe problematic.

Besides the implications of pregnant mom...folic acid...

Here comes watching HER vitamin D level (read just the last sentence or all):

http://www.sciencedaily.com/releases/2014/02/140226110836.htm

2014...

We are still figuring out "stuff"....including ME!

Ancora Imparo = "I am still learning."

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Eight Legs Bad
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Actually, I am highly skeptical of the studies by Denialists like Sigal et al where they try to imply that positive results on antibody tests showing binding to flagellar antigens (band 41 and derivatives) in patients with neuroborreliosis is due to cross-reaction with human HSP60, provoking auto-immunity.

The monoclonal antibody H9724, used by the Bowen lab to detect antigen in Lyme patients, and by Dr MacDonald in his early work with autopsy Alzheimer brain tissue, detected Borrelia infection in living and deceased patients.

The Denialists imply that these results are invalid and that it's just cross-reaction with human HSP60.

They lobbied to get Bowen lab shut down, but many patients positive on their blood test later had confirmation via other testing.

As for Dr MacDonald's results detecting borrelia in Alzhimer autopsy brain tissue with H9724, he later confirmed this using culture, PCR, and most recently - state-of-the-art Molecular Beacon DNA probes.

Bottom line - infection, not autoimmunity.

Elena

quote:
Originally posted by Marnie:
...However, some new research has indicated that HSP60 possibly plays a role in a “danger signal cascade” immune response.

There is also mounting evidence that it plays a role in autoimmune disease.



--------------------
Justice will be ours.

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surprise
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*whew* no wish to participate in your 'new theory' here Marnie,
but I can't help but comment:

The Hep B vaccination (a sexually transmitted disease!) that was given to my day old daughter, who weighed 6 pounds,

was given without my knowledge in the hospital where she was born within 24 hours of her birth.

And in the year 2005, that Hep B vaccine included mercury, along with a host of insidious toxins.

It certainly did NOT prevent her congenital Lyme disease from multiplying and descending upon her body.

Ridiculous.

--------------------
Lyme positive PCR blood, and
positive Bartonella henselae Igenex, 2011.
low positive Fry biofilm test, 2012.
Update 7/16- After extensive treatments,
doing okay!

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beaches
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Totally agree surprise. And ditto to the Hep B vaccine not preventing my kids from becoming horribly ill with Lyme Disease.

And since when can anyone administer a shot to an infant without parental consent? Outrageous!

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surprise
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Thanks Beaches for the support.

The consent for them to administer vaccines and whatnot was probably in legalese wording in the myriad of papers signed before hospital administration (and it was a planned C-section)

At any rate, I was trusting and uneducated about these sort of health issues (my much older son gratefully healthy and uncomplicated.)

It's Moms in the trenches like us who are making our real and painful experiences heard, despite media dogma to the contrary, that are making new mothers stop, pause, inform themselves, select, delay or say no, and protect their children.

--------------------
Lyme positive PCR blood, and
positive Bartonella henselae Igenex, 2011.
low positive Fry biofilm test, 2012.
Update 7/16- After extensive treatments,
doing okay!

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beaches
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I certainly hope the new moms are listening.

My oldest is at an age where I will have to start talking to her about all of this a some point soon. I know she will be receptive because she was so very, very sick.

It is really outrageous that in the many pages you had to sign for the c-section, there was likely hidden a page for Hep B vaccine.

That is deceptive IMO. When you are having a c-section, any and all consents should pertain to that, period.

Consents to vaccinate the baby should not be produced until after the child is born.

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hadlyme
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I've had the Hep B series of shots. Had them before I knew I had lyme and company.

Years after that series of Hep B shots, I then found out I had lyme. Which I have had for years before the Hep B shots.

When one works in healthcare, we were recommended in having the series. I never had any reactions to them, nor did they keep me from having lyme or anything with each related to each other in my opinion.

--------------------
Lyme, Babs, Fry Bug..... Whatever it is, may a treatment be discovered to make us all whole again!

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beaches
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hadlyme, I know those working in the healthcare field are mandated to have certain shots.

That's different from having a newborn vaccinated for Hep B shortly after leaving the womb, without an immune system.

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