Monday, December 26, 2016

Reovirus, beta-adrenergic receptors, aspirin, POTS, migraines, and aspirin sensitive asthma

This is a collection of noticeable overlaps of reoviruses, POTS, aspirin, migraines, and beta-adrenergic receptors.

reovirus receptor and beta-adrenergic receptors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC390558/

Beta-adrenergic receptors have been subdivided into three types
https://www.ncbi.nlm.nih.gov/pubmed/15170407

aspirin decreases the number of beta-adrenergic receptors? only in aspirin sensitive asthma?
https://www.ncbi.nlm.nih.gov/pubmed/8012645

high incidence of migraine in aspirin-sensitive-asthma
https://www.ncbi.nlm.nih.gov/pubmed/4003223

aspirin treatment for migraine
http://www.everydayhealth.com/pain-management/headache/aspirin-for-headache.aspx

I had previous looked at POTS and reoviruses
http://angelabiggs.blogspot.com/2016/08/postural-orthostatic-tachycardia_29.html

POTS and migraine
http://www.headaches.org/2015/05/04/migraineurs-frequently-experience-pots/

Migraine and HLA-DQ (the HLA connected with cytosolic viruses like reoviruses)
https://www.ncbi.nlm.nih.gov/pubmed/18345414

POTS and asthma
http://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2013.187.1_MeetingAbstracts.A2724

( note that there exists more than one type of asthma )

Is this reovirus, aspirin, and POTS relationship real??

note that ginkgo biloba decreases beta-adrenergic receptors
https://www.ncbi.nlm.nih.gov/pubmed/12203273

ginko has been thought to help migraine with aura
https://www.ncbi.nlm.nih.gov/pubmed/19415441

adrenergic receptor and genetic temporal lobe epilepsy
https://www.ncbi.nlm.nih.gov/pubmed/9855534

temporal lobe epilepsy and POTS
https://www.ncbi.nlm.nih.gov/pubmed/12662611

Celiac disease has also been connected with HLA-DQ (like migraine)

migraine and celiac
https://www.ncbi.nlm.nih.gov/pubmed/23126519

POTS and celiac
http://forums.phoenixrising.me/index.php?threads/study-finds-association-between-pots-and-celiac-disease-ncgi.46782/

If it was a reovirus that triggered the celiac disease it is possible that it eventually crosses over into the body and causes these other conditions.





Friday, December 23, 2016

Primary progressive MS, polyomavirus, CD20, and Orcerlizumab

The reason the new drug ocrelizumab works is because this form of multiple sclerosis was triggered by a polyomavirus cross-targeting with a larger infection (mycobacteria or staph).

Polyomavirus and CD20
https://www.ncbi.nlm.nih.gov/pubmed/11349723

Ocrelizumab is an anti-CD20
https://en.wikipedia.org/wiki/Ocrelizumab

Primary progressive MS : polyomavirus  (hepatitis B, JC, BK) HLA-C
https://healthimpactnews.com/2014/new-study-hepatitis-b-vaccination-in-france-sparked-a-wave-of-new-cases-of-ms/

previous blog post about multiple sclerosis
http://angelabiggs.blogspot.com/2016/11/the-4-types-of-ms-viruses-and-hlas.html

Autoimmune cross-targeting hypothesis:

The layering of 2 different infections on one target cell type triggers autoimmune disease.  A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria, or spirochete infection marking the outside.

Note that a vaccine can trigger autoimmune disease by attracting the immune system to the receptor the virus would bind unless that piece is removed from the vaccine.

France and hepatitis B vaccine triggering MS
https://healthimpactnews.com/2014/new-study-hepatitis-b-vaccination-in-france-sparked-a-wave-of-new-cases-of-ms/

virus receptor binding
http://angelabiggs.blogspot.com/2016/12/viruses-and-benzene-rings.html

The infections are not causing the autoimmune disease it is the immune system which is uncoupled with a cross-targeting issue.  Both the T cells and the B cells self educations cannot be turned off at the same time. 

Tuesday, December 20, 2016

HLA location hypothesis and the TLR location hypothesis

Title :

HLA location hypothesis

Abstract:

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

Introduction:

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.  Viruses have been suspected of triggering autoimmune disease.  When the HLAs and the viruses for an autoimmune disease are matched up patterns emerge revealing that different HLAs represent different areas of the cell.


Hypothesis:

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

All HLA-Ds are expressed by APCs

HLA-DR the cytosol (encapsulated virus or foreign protein)
HLA-DQ the cytosol (not an encapsulated virus)
HLA-DP the plasma membrane (outside of cell)

After NK attack the infected cell's cytosol is visible to APCs


Analysis of Hypothesis:

 Specific HLAs have been associated with genetic susceptibility to particular autoimmune diseases.  These same autoimmune diseases have also been associated with viral triggers. The purpose of an HLA is to bind foreign viral pieces and display them mailbox like to Tcells which means we can link the HLAs to the viruses.

When you look at an autoimmune disease, like alopecia for example, with the known HLAs and the suspected viral triggers you notice a pattern.  Considering where inside the cell these viruses end up a pattern emerged. Herpes alpha viruses infect the mitochondria. Polyomaviruses infect the endoplasmic reticulum.  Herpes gamma and beta viruses infect the nucleus.  Flu viruses and flavivurses infect the cytosol.

HLA-DQ : Reovirus : Areata Alopecia
HLA-C : Polyomavirus: Universalis Alopecia
HLA-DR4 : 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

Multiple sclerosis

HLA-B: Herpes-alpha (zoster): Relapsing remitting
HLA-DR15 : Flavivirus (hepatitis C/dengue ) :Secondary progressive
HLA-A: Herpes-gamma (epstein barr): progressive relapsing
HLA-C: Polyomavirus (hepatitis B/ JC, BK) : primary progressive

Which could mean that:

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 (APC)

The locations of the HLAs can be further verified by the genes and protein sequences of the HLAs themselves.  

HLA-As are linked to viral infections that infect the nucleus like HPVs or 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-A genes appear to be linked to the autosomal dominate spinocerebellar ataxia.  The syne-1 mutation which is linked to the recessive spinocerebellar ataxia is located on chromosome 6 right next to HLA-A. The Syne-1 gene makes the nesprin-1 protein which connects the cytosolic cytoskeleton to the nuclear membrane.  Is the HLA-A also a nuclear protein? Is this relationship significant?

Nuclear leader sequences contain very basic lysine and arginine sequences.  HLA-A, HLA-B, and HLA-C all contain a RRKSS sequence that is missing from HLA-D.  Since this sequence is conserved it could prove to be the nuclear sequence that HLA-A uses to get to the nucleus.

HLA-Bs don't use their nuclear sequence because they have a more dominant location sequence, a mitochondrial one. Mitochondrial sequences are the hydroxyl amino acids otherwise known as water-loving amino acids.  Serine, threonine, and tyrosine all have an OH group. The HLA-B protein at first glance does not have a mitochondrial sequence but there does exist a sequence that could become one.   HLA-B genes have been linked to the steroid 21-hydroxylase gene on chromosome 6.  These genes are right next to each other.  When this 21-hydroxylase enzyme is expressed it converts alanine to serine and valine to threonine.  The end sequence of the HLA-B protein "VS-L-TA" would become "TS-L-TS" which is a mitochondrial location sequence.

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 nerve 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-Bs can also be linked to viral, fungal, or bacterial proteins that find their way to the host's mitochondria and cause disfunction.

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 and may be using the serotonin or similar receptors to get there.

Newly translated HLA-Cs never use their nuclear sequence because they don't leave the endoplasmic reticulum. HLA-Cs have been found to bind tight to the ER proteins called TAP which is short for "transporter associated with antigen processing".  HLA-A and HLA-B only bound weakly to TAP and were able to leave the endoplasmic reticulum.  Further the gene for TAP has also been found on chromosome 6 near the HLA-C gene.

Which brings us to the HLA genes at the bottom of Chromosome 6 that do not have endoplasmic reticulum sequences or nuclear sequences. Are 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 the HLA-DRs are further divided up by numbers it is obvious that certain mailboxes grab certain viruses.  Just knowing the HLA mailbox associated with a disease could help predict which viruses could are involved.

HLAs can pick up anything foreign material not just viruses. Viral proteins, bacterial proteins, fungal proteins, and even medications will be picked up. What is interesting here is that the non viral associated HLAs  seemed to be connecting in other ways. For example when examining a few of the HLA-Bs, the exact foreign protein was not the same between infections but the effect on the the mitochondria appeared to be matching.  Apoptosis and oxidative stress seemed linked to HLA-B49 but when the mitochondria was in a state of fission from the foreign protein HLA-B8 was used.  The exact HLA mailbox could be telling us even more information than the where in the cell but what is happening.

Further note that HLAs that interact with T cells are glycosylated.  Is this how they end up outside of the cell?  When these HLA mailboxes bind their antigens is there a conformation change that allows glycosylation? Sugars are the instructions on membrane proteins indicating which sections are not in the cytosol.  Are HLAs on the inside until they have glycosylation, large sugars attached, and then they are pushed to the outside of the cell?

HLA-DPs are on the antigen presenting cells binding things that are outside of cells (until broken down by macrophages etc).  HLA-DPs hold the antigens of large infections or the viral coats.  HLA-DPs also bind to MHCIIs (HLA-DQ or HLA-DR) stabilizing them until it binds it's antigen.

http://www.uniprot.org/uniprot/P20036

Conclusion:
The location of the HLAs can be confirmed two ways. HLAs can be matched up with the viruses they bind which reveal where the HLA is because the virus infects that area of the cell. HLA genes and protein sequences themselves have telling relationships that reveal where the HLA belongs.


Title:
Toll-like receptor location hypothesis

Abstract:
The internal TLRs match up with the internal HLAs.  The internal TLRs identify foreign material inside the cytosol, mitochondria, nucleus, and the endoplasmic reticulum.  These TLRs have corresponding IFNs which when released trigger the corresponding HLAs for specific locations inside the cell and the appropriate TAMs to be worn by the macrophages.

Introduction:
TLRs are the innate immune system nets that catch large groups of foreign material.  Unlike the HLAs which grab and display specific antigens; TLRs catch broader groups.  TLRs were initially found to grab generic bacterial components.  TLR5s bind flagallins, TLR1s bind peptidoglycans of yeast and bacteria, TLR4 binds the sugars on gram negative bacteria and mycobacterias, and TLR6 binds the proteins of gram positive bacteria.  The internal TLRs seem to be binding DNA and RNA components.  What are the internal TLRS? TLR3, TLR9, TLR7, and TLR8.

Hypothesis:
The internal TLRs are location specific and trigger specific IFNs which trigger the corresponding HLAs for that same location, the NK cells, and tell the macrophages which TAM arms to wear.

Analysis of hypothesis:

Looking at each of the internal TLRs, which viruses they catch like generic nets, and which IFN is then expressed as a result reveals where each TLR is.  To begin with TLR3, TLR7, TLR8, and TLR9 are all found intracellularly.

TLR3 : cytosolic viruses:         IFN beta:       HLA-D :  TAM- TYRO3
TLR7: nuclear viruses:            IFN alpha:      HLA-A :  TAM-MER
TLR9: mitochondrial viruses: IFN alpha:      HLA-B :  TAM-MER
TLR8: endoplasmic reticulum: IFN gamma: HLA-C :  TAM- AXL

IFN gamma is made primarily by Natural Killer T cells.  Natural Killer cells strike when no TLRs or HLAs are visible on the cell's surface. These proteins are processed in the endoplasmic reticulum.    When the endoplasmic reticulum (ER) is infected with a virus there would be an issue with TLR8 or HLA-C ever making it to the surface of the cell.  If they can't make it to the surface IFN might not be made but the Natural Killer cells have evolved to compensate for these ER viruses.

The other zones of the cell have a simple pattern of the TLR net catching a virus and then the corresponding IFN. Here are some possible scenarios.

The flu virus is caught by TLR3 which then causes IFNbeta to be made.  As the infected cell secretes IFNbeta the natural killer cells (NKs) are drawn to the area to kill the infected cells.  Neighboring cells see the IFN and react.  Antigen presenting cells start producing HLA-Ds to diagnose exactly which cytosol virus pours out of the cell and the macrophages start to express the correct TAM.   The flu virus would then be grabbed with a very specific mailbox HLA-DR4. The HLA-DR4 would then present it to a T cytotoxic cell.  The macrophages would put on the TYRO3 TAM hand allowing it to eat self cells that are infected.

The Epstein Barr Virus is a nuclear virus which would be caught by TLR7 and IFNalpha is secreted.  When the Natural killer T cell breaks open these infected cells secreting IFN the virus will still be hidden inside the nucleus. The Antigen presenting cells are not the ones to told to express HLA-A because they can't see anything while the cells at risk in the area are told to do so.  The IFN alpha also tells the macrophages to wear the MER TAM hands.





And the IFN can connect to the TAMs...the macrophage hands.
http://angelabiggs.blogspot.com/2017/02/tam-receptors-and-ifns.html

















Wednesday, December 7, 2016

Zika could be using ACTH receptors: causing microcephaly and glaucoma!!

congenital glaucoma and steroid ACTH
https://www.ncbi.nlm.nih.gov/pubmed/16874997

zika causing glaucoma
https://www.sciencedaily.com/releases/2016/11/161130132813.htm

Microcephaly and Zika

Flaviviruses could be using melanocortin receptors.  Zika must have chosen the MCR2 receptor as it's main receptor.  MCR2 is also the ACTH receptor. ACTH is the first hormone used by the babies brain to grow.

melatonin protecting against flavivirus infection through competition with the receptors?
http://www.ncbi.nlm.nih.gov/pubmed/14962057

Zika and melanocortin receptors
http://angelabiggs.blogspot.com/2016/01/does-zika-virus-use-melanocortin.html

ACTH receptors are on the placenta which is how this virus crosses better than the others and ACTH is the critical baby's brain growth hormone.

Calcium and ACTH
http://www.ncbi.nlm.nih.gov/pubmed/6284662
http://www.ncbi.nlm.nih.gov/pubmed/4323934

Pituitary cushing disease which has the characteristic of high ACTH from a tumor  has calcium deposits...which makes you wonder what the displaced ACTH is doing if the virus uses the ACTH receptor.  This could explain the calcium deposits in the brains of babies with Zika.

Autoimmune cross-targeting hypothesis

The layering of 2 different infections on one target triggering autoimmune disease.  A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria infection marking the outside.

Zika + campylobacteria/sutterella at the peripheral nerves = guillian barre
Zika + staph at the CNS = acute flaccid paralysis
Zika + strep at the brain = encephalitis
Zika + mycobacteria at the substantia nigra = parkinson's
Zika + spirochetes like H.pylori at the bone marrow = Idopathic thrombocytopenic purpura 

There are blog posts for these containing reference links.

Co-carcinogenesis 

Rous' hypothesis requires a virus and a carcinogen together to start cancer.  My co-carcinogenesis takes his further:  Carcinogens inhibit polymerases. (yes we have been told carcinogens cause DNA damage but I think their ability to inhibit polymerases causes most cancer. The cancers have patterns and are not that chaotic)

Alone a carcinogen would inhibit growth until a virus appears opens up the DNA and modifies the cell by binding telomeres, to create virus supplies forever.  The problem is the carcinogen inhibits the viral polymerase better than the human polymerase.  So instead of the virus making what it wants the infected cell is transformed into a cancer cell.

Zika + benzene at the  bone marrow = leukemia

Zika  + PCB at the prostate = prostate cancer???


Cross-targeting triggering Rheumatoid arthritis. Can the HLAs reveal the viruses

Autoimmune cross-targeting hypothesis

The layering of 2 different infections on one target triggering autoimmune disease.  A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria infection marking the outside.

Rheumatoid arthritis would be mycoplasmas marking the outside of the tendon then a virus marking the inside.

mycoplasmas and rheumatoid arthritis
https://www.ncbi.nlm.nih.gov/pubmed/11128659
https://www.ncbi.nlm.nih.gov/pubmed/8943749
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1006269/?page=1
https://www.ncbi.nlm.nih.gov/pubmed/4948122

mycoplasmas and tendons
https://www.ncbi.nlm.nih.gov/pubmed/18766866
https://www.ncbi.nlm.nih.gov/pubmed/18766674

Sjogren's would not be mycoplasmas rather candida marking the outside then a virus on the inside.

Sjogren's and candida
https://www.ncbi.nlm.nih.gov/pubmed/21844143

HLA are the the T cell mailboxes that show what foreign things are inside the cell which often times is a virus.  Viruses infect different areas of the cell and tend to be grabbed by the same mailbox HLA.

HLA-A nucleus
HLA-B mitochondria
HLA-C endoplasmic reticulum
HLA-DR encapsulated virus in cytosol on antigen presenting cell
HLA-DQ non encapsulated virus in cytosol on antigen presenting cell
HLA-DP antigen presenting cells' HLA on surface plasma membraine

note that when the infected cell is popped...the APC still cannot see inside the nucleus, the mitochondria or ER membranes which is why the HLAs are there


HLA- DR 
Rheumatoid vasculitis HLA-DR4 flu
https://www.ncbi.nlm.nih.gov/pubmed/16762149

Rheumatoid vasculitis after flu vaccine
http://rheumatology.oxfordjournals.org/content/42/7/907.full

 rheumatoid and SJ with raynaud's has HLA-dr4
https://www.ncbi.nlm.nih.gov/pubmed/6605120

high RF

diabetes and rheumatoid (both can be triggered by the flu)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768389/

Flu viruses use dopamine receptors

Tendons and dopamine ?? parkinson's and tendon issues
http://ama.ba/index.php/ama/article/viewFile/159/pdf

Parkinson's caused by Rheumatoid drug
https://academic.oup.com/rheumatology/article/42/5/702/1784801/Severe-Parkinson-s-disease-in-rheumatoid-arthritis

Infliximab or remicade binds TNF alpha which is made not just by macrophages but my neurons

If the flu is still there marking the inside of the substantia nigra (infected through dopamine receptors) and then suddenly a foreign compound marks the outside of the cells because of the TNFalpha  it is possible that cross-targeting could occur causing the parkinson's following RA...but the key is the flu virus is still there and active when the remicade like drug is given.



HLA-A
Rheumatoid with lupus linked HLA-A2 EBV (HLA-A3 CMV)

high RF
ANA anti-nuclear antibody

HLA-All and lupus (HLA-All and CMV)
https://www.ncbi.nlm.nih.gov/pubmed/21658414

EBV and lupus
https://www.ncbi.nlm.nih.gov/pubmed/17121489

EBV use alpha estrogen receptors and CMV uses estrogen-like receptors.

Tendons and estrogen
https://www.ncbi.nlm.nih.gov/pubmed/18845777

Note that other viruses could possibly trigger RA but the HLAs should match up.  Here's a previous blog post where i was looking at retroviruses
http://angelabiggs.blogspot.com/2016/10/rheumatoid-arthritis-hla-drb1-and_24.html




CRP C-reactive protein : produced in the liver during inflammation

ANA anti-nuclear antibody

RF is an antibody directed against an antibody

ESR erythrocyte sedimentation rate

Is Language impairment and dyslexia connected to HLA-A3 and CMV / EBV ?

HLA and specific language impairment
https://jneurodevdisorders.biomedcentral.com/articles/10.1186/1866-1955-6-1

HLA-A1 short term memory issues
HLA-A3 expressive language ability problems
HLA-B8 and HLA-DQ receptive language issues

handedness and dyslexia
https://www.ncbi.nlm.nih.gov/pubmed/1574158
https://www.ncbi.nlm.nih.gov/pubmed/8533054

Many babies exposed to CMV have been shown to develop dyslexia
http://www.congenitalcmv.org/preschool.pdf

auditory neuropathy in infant after cmv infection
http://www.ncbi.nlm.nih.gov/pubmed/22789691

images of viruses infecting the brain
http://www.neurology.org/content/70/1/84.full.pdf


HLA-A3 and Progressive relapsing multiple sclerosis

progressive relapsing multiple sclerosis  expressive language issues
https://www.ncbi.nlm.nih.gov/pubmed/23374023

relapsing remitting multiple sclerosis and acute aphasia
https://www.ncbi.nlm.nih.gov/pubmed/15037704


Progressive relapsing:

Herpes-gamma (epstein barr) herpes-beta ( HHV6 )  HLA-A3

HLA-A3 and MS
https://www.ncbi.nlm.nih.gov/pubmed/993587
https://www.ncbi.nlm.nih.gov/pubmed/901638
https://www.ncbi.nlm.nih.gov/pubmed/2273414

ms and epstein barr
http://nn.neurology.org/content/3/5/e275.full.pdf
https://www.ncbi.nlm.nih.gov/pubmed/27725113
http://www.news-medical.net/news/20120106/Study-shows-how-Epstein-Barr-virus-triggers-MS.aspx

MS and HHV6 (herpes-beta)
https://www.ncbi.nlm.nih.gov/pubmed/20926836
https://www.ncbi.nlm.nih.gov/pubmed/21524958

seasonal MS relapses in italy
http://bmcneurol.biomedcentral.com/articles/10.1186/1471-2377-10-105

seasonal epstein barr
https://www.ncbi.nlm.nih.gov/pubmed/14520445

Relapsing remitting

Relapsing-remitting: Herpes-alpha (zoster family)/HSV1   HLA-B
https://www.ncbi.nlm.nih.gov/pubmed/1831772
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931768/

Herpes zoster is a herpes-alpha virus which uses the beta-estrogen receptor. Beta-estrogen receptors cycle to the mitochondria which means that bursts of estrogen could reawaken the virus (mostly women)

this form of MS involves mitochondrial dysfunction
https://www.ncbi.nlm.nih.gov/pubmed/12559505
https://www.ncbi.nlm.nih.gov/pubmed/16392116/
https://www.ncbi.nlm.nih.gov/pubmed/19293237

(probably overlaps with alzheimer's)

HSV1 has been linked to spatial learning issues
http://ns.umich.edu/new/releases/21854-herpes-viruses-associated-with-cognitive-impairment




The 5 types of Psoriasis ( what is known)

1. Plaque psoriasis or psoriasis vulgaris  - Mycobacteria

overlaps with psoriatic arthritis, crohn's, type 2 diabetes, high cholesterol

2. Erthrodermic psoriasis - specific mycobacteria tuberculosis

https://www.ncbi.nlm.nih.gov/pubmed/25120233

causes reddening, pain, and large skin shedding

3. Guttate Psoriasis - Strep infection (impetigo)

feels like sandpaper

4. Inverse Psoriasis - candida

diaper rash, sweat zones, very red and raw in creases

5. Pustular psoriasis or impetigo herpetiformis - staph. aureus

pus filled bumps (white blood cells)  of childhood or pregnancy which appears to be triggered by staph reacting to hormone fluxes, aspirin derivatives, and psoriasis medication

associated with eczema or atopic dermatitis (constant staph infections?)

note that staph has been shown to be sensitive to aspirin
http://dartmed.dartmouth.edu/winter03/html/vs_aspirin.shtml 









Tuesday, December 6, 2016

Receptor hypothesis: Understanding Viruses, Benzene rings, and disulfide bridges could help improve vaccine safety.


Having paired up viruses and receptors one can then divide them into two groups.  The benzene negative group and the nitrogen positive group.

 Recognizing the charge used by viruses to bind receptors will be vital in the "cleaning up" of vaccines.  Vaccines are still triggering autoimmune diseases like live viruses only because the piece of the virus that binds the receptor is still there in the vaccine.  Remove this binding piece and the danger of vaccines triggering could be removed....or at least that is my hope.

The negative group 

HPV - cannabinoid receptors
Flaviviruses - melanocortin receptors
Flu - dopamine receptors
Herpes viruses - estrogen receptors
Polyomaviruses - vit D receptors


?Retroviruses - LH/ albumin receptors?

The herpes' benzene ring recognizes the estrogen receptor.
https://www.ncbi.nlm.nih.gov/pubmed/11137303

The Vitamin D does not have a ring it has 2 double bonds in the middle of the molecule.  Aflatoxin which uses vit D receptors does have a benzene ring in the middle of the molecule where vit D has the 2 double bonds.  Polyomaviruses use the vit D receptor.

Zika, melanocortin receptors, and  clatherin inhibitors
http://angelabiggs.blogspot.com/2017/01/zika-acth-receptors-and-clatherin.html


The positive group

Now the enteroviruses, paramyxoviruses, and rhinoviruses do not have benzene rings but have instead a positively charged nitrogen typically on a conserved lysine.

Note that acetylcholine and nicotine have an O-c-c-N pattern. (oxygen- carbon-carbon- nitrogen).  This should be looked for on Paramyxoviruses. (the positively charged Nitrogen is key)

The Acetylcholine receptors and the ICAM-1 (intercellular adhesion molecule) all have conserved disulfide bridges which appear to be serving as the electro-negative draw for the nitrogens.

Enteroviruses - nicotine acetylcholine receptors
Paramyxoviruses- muscarinic acetylcholine receptors
Rhinoviruses- ICAM-1

Charged molecules are drawn to the receptors and the virus must being do this too with a similar amino acid key.

Rhinovirus...conserved lysine in loop involved in binding
https://www.ncbi.nlm.nih.gov/pubmed/12768011

charge interactions between ICAM1 and rhinoviruses
https://www.ncbi.nlm.nih.gov/pubmed/10600561

ICMA-1 has disulfide bridges

Acetylcholine receptors and disulfide bridges
https://www.ncbi.nlm.nih.gov/pubmed/17132687

The receptor D68 uses must have sialic acid
https://www.ncbi.nlm.nih.gov/pubmed/26787879
https://www.ncbi.nlm.nih.gov/pubmed/26563423

nicotine receptors have sialic acid
https://www.ncbi.nlm.nih.gov/pubmed/20487973

Could the use of nicotine patches could slow the paralysis of patients?

corona viruses use the ace receptors and are said to use sialic acid to bind....where do they fit in this?


Sunday, December 4, 2016

Puzzling out the herpes viruses and the estrogen receptors

CMV has an extra coating on capsid in cytosol
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC356711/pdf/jvirol00262-0261.pdf

CMV and Herpes simplex both cross the plasma membrane by fusion and move across cytoplasm to the nuclear pore
https://www.ncbi.nlm.nih.gov/pubmed/4370986

Is it in the cytosol that they bind to estrogen receptors?

Estrogen receptor locations
https://www.ncbi.nlm.nih.gov/pubmed/3695480

herpes and estrogen receptors
https://www.ncbi.nlm.nih.gov/pubmed/19846508

Heavy metals and estrogen receptors
https://www.ncbi.nlm.nih.gov/pubmed/10770491
https://www.ncbi.nlm.nih.gov/pubmed/12746304

The beta estrogen receptors move into the mitochondria while the alpha and the estrogen like move into the nucleus.

previous blog post
http://angelabiggs.blogspot.com/2016/08/attempting-to-match-up-herpes-viruses.html

Alpha-herpes viruses: Herpes simplex 1, herpes simplex 2,  herpes zoster : Estrogen-beta receptors (nerves and uterine tissue)

Beta-herpes viruses: CMV, HHV6, HHV7 :  Estrogen-related receptors (CMV binding confirmed)

Gamma-herpes viruses: EBV, HHV8 : Estrogen-alpha receptors (lymphocytes, breast involved)

CMV compared to herpes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC356711/pdf/jvirol00262-0261.pdf
Herpes disrupts the plasma membrane while CMV does not. CMV had dense cytoplasmic bodies where as herpes viruses did not. (CMV binds the estrogen like receptor)

Herpes viruses and glycoproteins???
https://www.ncbi.nlm.nih.gov/pubmed/9770079

so do the capsid become imbedded in the plasma membrane first ? then release into the the cytoplasm without the coat? Where it then binds with the estrogen receptors?


HLA-DP2 and viruses like CMV ?
https://www.ncbi.nlm.nih.gov/pubmed/22797815

are these viruses with aromatic amino acid coats?