Monday, October 24, 2016

Rheumatoid arthritis, HLA-DRB1, and retroviruses...or is it EBV or a parvovirus? Does HLA-DRB mean cytosolic viral DNA?

Using the HLA-location hypothesis one would match HLA-DRB1 to retroviruses
Which retrovirus can trigger arthritis but EBV has been the virus constant identified in the area.

hypothesis of retroviruses and RA

retroviruses induce arthritis in goats

High seroprevalence of HTLV in RA (oligoarthritis knee type?)

HLA-dr1 and HLA-dr4

HLA-DR is the mailbox for the cytosol typically matched with encapsulated cytosolic viruses

rheumatic heart disease

EBV uses alpha-estrogen receptors which typically move to the nucleus....unless we are talking about synovial cells

EBV in nucleus and cytosol of monocytes

in Synovial cells the estrogen-alpha receptors can be found in  the cytosol

Retroviruses are RNA viruses that become DNA in the cytosol so it matches but why would EBV DNA virus in the cytosol ?

Does the B part of HLA-DRB signify DNA in the cytosol?

Here is the older post of mycoplasmas and EBV:

Autoimmune cross-targeting hypothesis: a virus marks the inside of a cell while a larger infection marks the outside and the combination triggers autoimmune disease.  The immune system is instructed to destroy both the inside and the outside of the target.

The target of Rheumatoid arthritis might be the synoviocyte cells with mycoplasmas marking the outside and EBV marking the inside. ( I have changed the target tissue to tendons since this post was made but obviously more than the tendons are getting infected)

Fibroblast-like synoviocyte, mycoplasmas, and Rheumatoid arthritis

EBV detected in synoviocyte of Rheumatic patients (review)

With the associations of plantars fascititis, carpal tunnel, morning stiffness, and the visible inflammation of tendons I am leaning toward the tendons as the autoimmune tissue target of rheumatoid arthritis.

Tendons were the first suspected target in 1969

interesting note: resveratrol (red grapes and blue berries) is an antagonist for alpha-estrogen receptors (not beta)

some people have notice resveratrol helping their arthritis which would give support to EBV triggering some forms of RA because EBV uses the alpha receptor.

What bothers me is that ER alpha receptors would go the the nucleus and interact with the DNA. Unless Tendon's have their own version of alpha-estrogen receptors which stay in the cytosol.

This book suggested that tendons have their own version of alpha-estrogen receptors.

If some estrogen receptors stay in the cytosol and have other purposes this would explain what is going on.

Another virus that triggers RA is the parvovirus

parvovirus and arthritis

Parvovirus, arthritis, and HLA-DRB1

note that the parvovirus is a DNA virus (supports the DRB idea)

Raynaud's might be triggered by B19 erythrovirus (parvovirus in humans)

Friday, October 21, 2016

HLA Location hypothesis

Title :

HLA location hypothesis


 HLAs identify not just the foreign antigen from inside the cell but where in the cell, which organelle, the antigen was found.


Human leukocyte antigens, HLAs, are cell surface proteins that serve as mailboxes to T cells.  T cells having been educated in the thymus to know all internal cell self antigens thus would react to foreign antigens presented in these HLA mailboxes.   Currently HLAs have been recognized as reflecting genetic susceptibility to various autoimmune diseases.

HLAs identify not just the foreign antigen from inside the cell but where in the cell, which organelle, the antigen was found.  When the patterns of the HLAs in autoimmune diseases are looked at with the suspected viral triggers a pattern emerges suggesting that the type of HLA reflects the location within the cell because viruses only infect certain areas within the cell.  

HLA-A the nucleus
HLA-B the mitochondria
HLA-C the endoplasmic reticulum
HLA-DR the cytosol (encapsulated virus)
HLA-DQ the cytosol (not an encapsulated virus)
HLA-DP the plasma membrane/ endocytosis

Analysis of Hypothesis:

HLA-As are linked to viral infections that infect the nucleus like HPV and herpes-beta or herpes gamma viruses.  These viral infections are also linked to cancers because they infect the nucleus where they interfere with the DNA, the cell's cookbook.

HLA-Bs are linked to viral infections that infect the mitochondrial such as the herpes-alpha viruses.  Herpes zoster specifically is known to travel down the nerves in the mitochondria like a little car during shingles infections.  As the nerves branch out the viral infection does too infecting the next nerves in the line.

HLA-Cs are linked to polyomaviruses which infect the endoplasmic reticulum.  Hepatitis B, JC, and BK viruses are found in the endoplasmic reticulum during infection.

 Finally the HLA-D mailboxes are linked to viruses in the cytosol. Reoviruses of celiac disease match up with HLA-DQ whereas the HLA-DR type of mailboxes appear to pick up viruses like the flu.  The distinction between these two types of viruses is encapsulation.

When you look at an autoimmune disease like alopecia for example with the known HLAs and the suspected viral triggers you notice a pattern.

HLA-DQ : Reovirus : Areata Alopecia
HLA-C : Polyomavirus: Universalis Alopecia
HLA-DR : Flu : Totalis Alopecia

The same thing can be done with parkinson's

Late onset sporadic parkinson's : flaviviruses or flu : HLA-DR
Parkinsonism with dementia/alzheimer's : herpes viruses HLA- A, B

( Note that the viral trigger is only half the cause of the autoimmune disease and that the larger infection on the outside can be linked to other diseases.  For instance mycobacterias which can be linked to parkinson's can also be linked to type 2 diabetes, psoriasis, high cholesterol, and even bipolar issues. Please see the autoimmune cross-targeting hypothesis for more information)

The HLAs continue to match of with viral families revealing fascinating patterns. For instance in multiple sclerosis the more common form seems to be connected to the Herpes alpha family which with increasing  the "chicken pox" vaccinations  of children may disappear.

Herpes-alpha (zoster family)  HLA-B
Polyomavirus (hepatitis B) HLA-C

Further since polyomaviruses appear to be using vitamin D receptors this is the group vitamin D supplements could have the biggest impact on.  Assuming the virus is still active in the autoimmune disease state.

Some flavivirus should be able to trigger HLA-A because the melanocortin-receptor-one cycles there and some of them may be involved in Cancer.

Spirochetes, high cortisone, and HLA-C w3

Previous considered spirochetes quorum, cortisone, and other thoughts

H.pylori and HLA-C w3

Lyme's Borreliosis and HLA-C w3

cleft palate and HLA-C w7

cortisone causes cleft palate

the cortisone reactions take place in the ER (not the cytosol)

If HLA-C is the Tcell mailbox for the ER what is w3 picking up from the spirochetes?  an endotoxin or cortisone ?

Thursday, October 20, 2016

Amyotrophic lateral sclerosis, HLA-c, the endoplasmic reticulum, the vit D receptor, and an aflatoxin-like compound

Is ALS triggered by aflatoxin like compounds and tau is produced? Previous post I am building on.

Trichophyton cencetricum and ALS...definitely connected but is autoimmune cross-targeting with herpes or is it from the aflatoxin like compound that is made that destroys the nerve?

Aflatoxin like compounds are made by some dermatophytes
specifically T.concetricum

Guam has high rates of ALS

High rates of trichophyton concentricum on Solomon children (close to guam and makes you wonder if both areas share this infection)

ALS and lakes in new england

Has this t.concentricum moved into these lakes?

aflatoxin binds the Vit D receptor

ALS is slowed with vit D supplements

Tau has been found to be reduced with vit D supplementation

Tau protein as a marker for ALS


HLA C3 and C4 and als

aflatoxin and the endoplasmic reticulum

HLA-C the mailbox for the endoplasmic is the HLA-C picking up aflatoxin?

aflatoxin uses the vit D receptor like polyomaviruses which then are picked up the HLA-C3 or HLA-C4 depending on which polyomavirus. (maybe the body get confused with aflatoxin and can't decide which virus it is, which it is not, so the immune system uses both?)

Wednesday, October 19, 2016

Does HLA-B27 bind the butyrolactones of Stenotrophomona bacteria or aspergillus fungus?

Fibromyalgia and ankylosing spondylitis

HLA-B27 and ankylosing spondylitis

fibromyalgia and HLA-B27

HLA and cushing

Stenotrophomonas possible connection to fibromyalgia and pituitary tumors. (my older posts)

butyrolacetones get into the mitochondria

the HLA-B is the mailbox for the mitochondria (HLA location hypothesis)

picks, ALS, asperger's, and aspergillus

aspergillus and butyrolacetones

asperger's and anklyosing

asperger's and pituitary tumors

Pick's disease and aspergillus

Do these diseases have HLA-27 linked to them because some forms of aspergillus use butyrolacetones?

Note that the sleep aid gamma-butyrolacetone can induce pituitary tumors

Also not that HLA-B27 is not specific to gamma-butyrolactones

Measles HLA-DR1 and HLA-B27

HLA-B27 and measles fusion protein

measles and mitochondrial dysfunction

Narcolepsy, HLAs, and the N1H1

Previously connect flu and strep to narcolepsy suggesting autoimmune cross-targeting

Now going back and seeing if the HLAs match up

narcolepsy and HLA-DR2

DR2 / DR4 H1N1 flu

flu and narcolepsy

Tuesday, October 18, 2016

HLA-B8 and host mitochondrial fission?

Does HLA-B8 mean that mitochondrial fission has occurred during an infection?

Several autoimmune diseases have been associated with HLA-B8. Celiac, DH, and graves have been associated with e.coli.  Addisons and SJ have been connected to candida infections.  (note that graves can be caused by a variety of bacterias)

The connection to HLA-b8 that stands out is hepatitis C.  What does this virus have in common with these infections? All of these infections and hepatitis C cause mitochondria fission.

HLA-B8 is a mitochondria does this mailbox signify not just something in the mitochondria of the host but that fact that fisson has occurred?

hepatitis C and hla-b8

hepatitis C and the mitochondria fission

(hepatitis C goes seems to go to the nucleus using MCR1 so how it causes the fission is not figured out)

e.coli and mitochondria fission

farsenol induces fragmentation of mitochondria (fission)

Farsenol is a quorum made by candida.

This mitochondrial fission is the only thing i can find connecting this infections with the mitochondria explaining the HLA-B8.

 Any other ideas?