Hypotheses: Autoimmune Cross-targeting, Co-carcinogenesis, and Quorum complications : June 2017

Wednesday, June 28, 2017

Comparing xanthomonas and spirochetes....and overlap of butyrolactones used as quorum?

Spirochetes look connected to vit C and cortisone levels
http://angelabiggs.blogspot.com/2016/06/does-hpylori-bind-to-sodium.html
http://angelabiggs.blogspot.com/2016/07/spirochetes-and-high-cortisol.html

Are they also connected weakly to butyrolactones?

Xanthomonas is a bacteria that infects nightshade plants. They use butyrolactones as signalling molecules between them.

In our bodies butyrolactones is converted to GHB which is then converted to GABA. GABA is the neurotransmitter. How our nerves talk to each other.

A form of Xanthomonas has been found to infect the respiratory tract of people and is considered a new bacterial genus: named Stenotrophomonas.

My notion is actually a question: does the Stenotrophomonas still make these signalling molecules when exposed to nightshades like a bell pepper when it infects us? Could this explain the painful reactions to nightshades that Fibromyalgia patients have? Are antibodies directed at the butyrolactones causing antibodies to GABA thus causing one's own immune system to attack our nerves?

Do spirochetes like lyme diseases' Borrelia bacteria use butyrolactones too? Maybe not continuously like Xanthomonas but at times? which is why vit C or vaccines can trigger the fibomyalgia like reactions in lyme disease patients?

Genes have been found to be shared between Xanthomonas and Borrelia.
https://www.ncbi.nlm.nih.gov/pubmed/?term=Borrelia+burgdorferi+Xanthomonas

Can is lyme disease a trigger of the same diseases as Xanthomonas? bone spurs, the fibromyalgia, pituitary tumors that GHB cause?

Xanthomonas are also called stenotrophomonas when they infect people

http://angelabiggs.blogspot.com/2015/11/stenotrophomonas-possible-connection-to.html

no pubmed ref connecting Borrelia to bone spurs but patient posts

"When I got Lyme symptoms last spring, I developed bone spurs in my right shoulder and knee almost over night. Recently I went off Banderol and Samento for 36 hours and had a bad herx.....joint pain, fatigue, depression, and I feel like I have developed bone spurs in my left shoulder. I get a popping noise when I put my arm behind my back, which I didn't have the day before. My upper and lower spine is also achy. I am not sure if the inflammation from Lyme has triggered an autoimmune disease. Has anyone else had this symptom? It seems to happen whenever I have a bad herx. I am detoxing with cucurmin, epsom salt baths, chorella, parsley, pinella, burbur, and sparga. Thanks for any advice."

fibromyalgia and borrelia
https://www.ncbi.nlm.nih.gov/pubmed/7573105

Collection of what might kill spirochetes http://angelabiggs.blogspot.com/2016/05/brassicaceae-mustards-mustard-flowers.html

Xanthomonas grows not just on nightshades like peppers but on wheat ,corn, soy and dairy....specifically lactose. It is the "black rot" of vegetables.

Does this mean that a person with Xanthomonas can develop a lactose sensitivity?

Xanthan gum is produced by the fermentation of glucose, sucrose, or lactose...but the type that infects people, Strenotrophomonas maltophilia cannot ferment lactose.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061566/

Wednesday, June 14, 2017

Alzheimer's and the dysfunctional mitochondria. Damage to the mitochondria causes Alzheimer's: methanol (aspartame creates this), diacetyl (artifical butter), and alpha herpes viruses (like the chicken pox virus)

Alpha-herpes viruses : HHV1, HHV2, HHV3 (zoster which is the chicken pox virus)

Alpha-herpe viruses destroy host's mitochondrial DNA
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1796774/

the alpha-herpes virus drives the mitochondria down the nerve root to other nerves!
http://www.sciencedirect.com/science/article/pii/S1931312812001047
herpes causes amyloid
http://www.ncbi.nlm.nih.gov/pubmed/17980964
http://www.ncbi.nlm.nih.gov/pubmed/16109164

Herpes and Alzheimer's Patients
http://www.ncbi.nlm.nih.gov/pubmed/18973185
http://www.ncbi.nlm.nih.gov/pubmed/22216291
http://www.ncbi.nlm.nih.gov/pubmed/18982063
http://www.ncbi.nlm.nih.gov/pubmed/23261465

Note that the herpes viruses may use estrogen beta receptors to get into the mitochondria.
reactivation of herpes virus is linked to the estrogen receptor
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2798450/

Imagine the herpes virus traveling down the nerve to the next one in little mitochondrial cars and breaking them as they go.

Mothers of kids with down syndrome and risk of alzheimer's (faulty mitochondria through age?)
http://www.ncbi.nlm.nih.gov/pubmed/7914304

Mothers give a grab bag of mitochondrias to their children. "the good, the bad, and the ugly" mitochondrias are randomly given to offspring. Sometimes more bad then good. A mother can develop Alzheimer's sooner but it depends on how many dysfunctional mitochondria she has.

Amyloidosis is the high with Agent orange patients
http://www.ncbi.nlm.nih.gov/pubmed/24906069

Auxins (agent orange chemicals) bind the mitochondria directly causing dysfunction
http://www.ncbi.nlm.nih.gov/pubmed/11566291

The Amyloid show up in the legs where people had been exposed to the chemical auxin and further supports the notion that when mitochondrias are broken that amyloid results.

Papers suggesting that amyloid and mitochondria connections
http://www.ncbi.nlm.nih.gov/pubmed/22833458
http://www.jneurosci.org/content/33/43/17042.short

Previous papers discussing Alzheimer's and mitochondrial dysfunction
http://www.sciencedirect.com/science/article/pii/S0925443909002427
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907118/
http://www.ncbi.nlm.nih.gov/pubmed/15193340
there are tons more but it is unclear why the mitochondria has issues

APP function...why does amyloid build up?
http://www.ncbi.nlm.nih.gov/pubmed/26274614

I had suggested that it was a serine protease growth key, a necessary function
http://angelabiggs.blogspot.com/2014/03/rescued-app-paper-from-alzforum-written.html
I need to figure out the date i wrote this for the forum.

APP triggering growth of colon cells
http://www.ncbi.nlm.nih.gov/pubmed/11279603

sAPP and neurite extentions
http://www.ncbi.nlm.nih.gov/pubmed/8083748
http://www.ncbi.nlm.nih.gov/pubmed/9110259

APP as a serine protease and neuroserpin?
http://www.ncbi.nlm.nih.gov/pubmed/16849336
http://www.ncbi.nlm.nih.gov/pubmed/19843463

Nitric oxide stops mitochondria of firefly
http://icb.oxfordjournals.org/content/44/3/213.long

NO and brain mitochondria
http://www.nature.com/nrm/journal/v3/n3/abs/nrm762.html

Now imagine in an active neuron the mitochondria car is moving quickly down the microtubular tracks to the synapse...NO would normally halt the movement. If the mitochondrias had not reached their destination would the synapse send an app signal in an attempt to keep the mitochondrias moving?

Amyloid-beta inhibits NO formation
http://www.jneurosci.org/content/25/29/6887.full
Is amyloid-beta the growth switch clipped because it is not working?

But if nitric oxide was not the reason the mitochondria wasn't moving....would amyloid-beta continue to be made and sent in desperation by the synapse? If herpes viruses were destroying the mitochondria would NO be low because of amyloid-beta?

Anti-herpes virus stuff

Arginine http://www.ncbi.nlm.nih.gov/pubmed/19288025
Vit C, ascorbic acid: http://www.ncbi.nlm.nih.gov/pubmed/18813862
Lemon balm: http://www.ncbi.nlm.nih.gov/pubmed/18693101

Lemon balm and alz memory
http://www.ncbi.nlm.nih.gov/pubmed/12888775

Tuesday, June 13, 2017

Mycoplasmas, boron, and TNF alpha?

Looking at "natural remedies" the mineral boron has claims to remedy rheumatoid arthritis. Boron deficiencies have associations similar to rheumatoid arthritis Is it possible that the "tip organelle" of mycoplasmas bind where boron does? Do mycoplasmas use boron receptors to infect ? Is it possible that THF is meant to not only recruit neutrophils but to compete with mycoplasmas for these boron receptors?

RA and low boron levels (how does the RF factor fit in?)
http://www.scopemed.org/?mno=26288

Boron and red blood cells
https://www.researchgate.net/publication/50951788_Dietary_boron_affects_blood_cell_counts_and_hemoglobin_concentrations_in_humans

RA and anemia
https://www.ncbi.nlm.nih.gov/pubmed/2180049

if boron binds heme could this somehow explain the anemia and photosensitivity of RA patients?
https://www.ncbi.nlm.nih.gov/pubmed/20576510

heme deficiency causes photosensitivity (there is a genetic link between genetically faulty hemes and photosensitivity )

boron and mycoplasmas (do not eat borax it is toxic)
http://www.jbbardot.com/inexpensive-osteoporosis-mycoplasma/

This Borax article suggests that boron somehow acts against mycoplasmas. It is the hypothesis of this blog that mycoplasmas use the Boron receptor. The connection to boron can be found in every area of RA.

mycoplasmas and rheumatoid arthritis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1006269/

Boron is used to produce bone (supplement is even given in osteoporosis)
https://medlineplus.gov/druginfo/natural/894.html

Rheumatoid and osteoporosis
http://www.webmd.com/rheumatoid-arthritis/rheumatoid-arthritis-and-osteoporosis#1

Boron and parathyroid
http://forums.phoenixrising.me/index.php?threads/boron-deficiency-causes-the-parathyroids-to-become-overactive.25880/

Rheumatoid and parathyroid
http://ard.bmj.com/content/71/Suppl_3/654.1

Boron is used by bones, joints, parathyroid, dental enamel, the thyroid, and the pancreas

Interestingly some forms of RA seems to affect the bones as osteoarthritis, overactive parathyroid, graves disease, and diabetes

mycoplasma's tip organelle
http://onlinelibrary.wiley.com/doi/10.1111/j.1574-6968.2001.tb10610.x/full

Mycoplasmas bind negative
https://www.researchgate.net/publication/51192733_Identification_of_Amino_Acid_Residues_Critical_for_Catalysis_of_Holliday_Junction_Resolution_by_Mycoplasma_genitalium_RecU

These tip organelles have a high concentration of adhesions which might function as a strong lewis acid because Boron is a strong lewis acid. Hypothesis: the mycoplasma are strong lewis acids. (this means they can accept an electron pair)

Boron and adhesives
https://www.researchgate.net/publication/266210033_Boring_Boron_and_Adhesives

Foods high in Boron : Raisins are the highest
https://www.algaecal.com/algaecal-ingredients/boron/boron-sources/
safer than the Borax

If TNF is the cytokine of warning of internal cell infections because it is released by macrophages:

Is it possible that THF is meant to not only recruit neutrophils but to compete with mycoplasmas for these boron receptors directly? When a macrophage itself is infected and can no longer function as the immune system vacuum it releases THF which suppresses FOXp3 which increases the Tcells looking for internal infections which would be viruses or mycoplasmas. TNF also recruits immune system macrophage like cells that do not have nucleuses like neutrophils. (no nucleus for a virus to infect) It is very likely that TNF would have developed a feature against mycoplasmas.

TNF high levels and lupus blood cell issues
http://lupusresearchinstitute.org/our-research/lri-researcher-discovers-cause-and-potential-treatment-approach-lupus-anemia

Does TNF alpha sort of fit into this too???

TNF is released by macrophages when they have succumbed to infection like mycoplasmas. Is it possible that a second action of TNF is to compete with mycoplasma binding? (not just to stimulate neutrophils)

TNF alpha bind negative
http://www.jimmunol.org/content/143/4/1192

TNF and bone
https://www.ncbi.nlm.nih.gov/pubmed/17350185

TNF and parathyroid
https://www.ncbi.nlm.nih.gov/pubmed/1325978

review of TNF drugs?
http://www.sciencedirect.com/science/article/pii/S1359610114000781

Enbrel (etanercept) binds the TNF alpha receptor
https://en.wikipedia.org/wiki/Etanercept

Humira (adalimumab) binds directly to the TNF alpha molecule and then floats around with it.

(humira is an IgG molecule)

TNFalpha if it is a lewis acid like boron would float around with humira and bind up Copper explaining the side affects of Humira.

Humira causes foot drop and copper deficiency

foot drop and copper deficiency (after bariatric surgery)
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000200232

Copper reacts with lewis acids
http://pubs.acs.org/doi/abs/10.1021/jo202624s

Nodules have been found with enbrel.
https://www.ncbi.nlm.nih.gov/pubmed/11920425
https://www.ncbi.nlm.nih.gov/pubmed/28357602

note that macrophages can also be infected by candida (fungal infections) which is why TNF occurs in Lupus, discord lupus and sj.
http://www.aspergillus.org.uk/content/how-does-candida-kill-macrophages

lupus vs. SJ ?
http://angelabiggs.blogspot.com/2014/09/lupus-vs-sjogren-can-you-seperate-them.html

This blog post is focused on the RA forms that are linked to mycoplasmas.

Considering Felty's syndrome and how this boron, THF, and mycoplasma competition could explain things.

boron: high in bone, thyroid, and.....spleen

Felty's syndrome : RA, splenomegaly, and neutropenia
https://www.ncbi.nlm.nih.gov/pubmed/21255689
https://www.ncbi.nlm.nih.gov/pubmed/10553980

Could the mycoplasma infect the spleen using boron receptors?

Neutropenia is the loss of neutrophils. THF released by infected macrophages triggers neutrophils.

Are the mycoplasmas infecting the neutrophils?

mycoplasmas and neutrophils
http://www.sciencedirect.com/science/article/pii/S0165242717302222

rheumatoid nodules are common in 75% of Felty patients
http://www.uptodate.com/contents/rheumatoid-nodules

Are the mycoplasmas blocking TNF receptors just like enbrel? but infecting using the boron receptors?

previous post
Dividing up the types of Rheumatoid arthritis further using HLAs and viruses
http://angelabiggs.blogspot.com/2016/12/cross-targeting-triggering-rheumatoid.html

Nodules are made up of excessive collagen. If nodules are caused by inflammation without TNF receptor activation what is happening? only the cytokine il-1 ?

cytokine il-1, RA nodules, and TNF
https://www.ncbi.nlm.nih.gov/books/NBK6288/

http://onlinelibrary.wiley.com/store/10.1002/art.10776/asset/10776_ftp.pdf?v=1&t=j41cc75s&s=3641ae28d7ef50302d0d55fdcc5fdafd65bc7b9f

Il-1 stimulates collagen growth in skin cells
http://www.sciencedirect.com/science/article/pii/0167488987901698

So the same thing must be happening in the tendon when the TNF receptor is blocked and only il-1 is seen by the tendon.

Hypothesis: When nodules form it is because the TNF receptor is blocked by anti-TNF receptor drugs or mycoplasma binding and the il-1 stimulates collagen growth unchecked

here humira caused nodules?
https://www.researchgate.net/publication/282068751_Adalimumab-induced_lupus_erythematosus_profundus_in_a_rheumatoid_arthritis_patient

does this mean that the floating complex adalimumab-THF still can bind the receptor?

panniculitis and enbrel study
http://factmed.com/study-ENBREL-causing-PANNICULITIS.php

review of TNF receptors (TNF R1 is the one involved with inflammation )

TNFR1 is involved in adipose cells
http://www.sciencedirect.com/science/article/pii/S0014579307011957

TNFR2 is on blood vessels cells

achilles tendon and THF alpha (TNFR1 seems involved)

https://www.researchgate.net/profile/James_Gaida/publication/224932188_Evidence_of_the_TNF-alpha_System_in_the_Human_Achilles_Tendon_Expression_of_TNF-alpha_and_TNF_Receptor_at_both_Protein_and_mRNA_Levels_in_the_Tenocytes/links/54ded6880cf2510fcee51da8/Evidence-of-the-TNF-alpha-System-in-the-Human-Achilles-Tendon-Expression-of-TNF-alpha-and-TNF-Receptor-at-both-Protein-and-mRNA-Levels-in-the-Tenocytes.pdf

Risk of heart failure is extremely high in RA patients

anti-TNF therapy seems protective against heart failure in RA patients
https://www.ncbi.nlm.nih.gov/pubmed/14984815

So what is happening in RA???? It starts as an infection of the tendons, mycoplasmas in at least 30%, and then a virus infects the tendon too trigger autoimmune cross-targeting.

http://angelabiggs.blogspot.com/2016/10/rheumatoid-arthritis-hla-drb1-and_24.html

Friday, June 9, 2017

updated: Virus families bind and enter cells using receptor families.

Hypothesis: Virus families bind and enter cells using receptor families.

Abstract: A review of literature shows that there is substantial evidence that virus families use receptor families.

Introduction: In 1982 Yale researchers led by Dr. Lentz began to suspect that the rabies virus bound acetylcholine receptors. Within a few years they had proven their suspicions and created the conceptual idea that the reason viruses do not infect all cell types was that viruses entered cells using different receptors like keys to doorknobs. Subsequent research matching viruses to receptors reveals the possibility that virus families use receptor families. The following paper will be a review of four virus families and the possible receptor families associated with them.

Analysis of Hypothesis:

Three viral families have substantial evidence connecting them to specific receptor families: Polyomaviruses, Herpes viruses, and Flaviviruses. The polyomaviruses BK and JC along with herpes virus HHV8 have direct evidence of binding to specific receptors. The Herpes viruses and flaviviruses have indirect but highly suggestive evidence of association with receptors that will be discussed.

Polyomaviruses may bind ganglioside receptors. The Bk virus has been found to bind ganglioside receptors. The JC virus has been found to bind serotonin receptors. Serotonin receptors had at one time been classified as a ganglioside receptor not the glycosphingolipid receptors. If serotonin binds both gangliosides and glycosphingolipids than a virus very likely binds both. Transgenic mice forced to express the SV40 virus have adaptively over expressed serotonin receptors. It is highly likely that this SV40 and other polyomaviruses also bind these ganglioside/serotonin receptors.

Herpes viruses may bind estrogen receptors. The HHV8, a gamma-herpes like EBV, has specifically been found to bind the alpha estrogen receptor. The other types of herpes viruses may bind the other estrogen receptors. Although binding has not been proven HHV1 a gamma-herpes has been found to be estrogen receptor dependent during infection. Also consider that the beta estrogen receptors cycle to the mitochondria which is where the alpha-herpes viruses like Herpes Zoster has been found. The EBV and CMV are found in the nucleus like the HHV8 which suggests that they use either the alpha estrogen receptors or the estrogen-related-receptors (like progesterone). Do gamma-herpes use alpha receptors, alpha-herpes use beta-estrogen receptors, and beta-herpes use estrogen-related receptors?

Considering reactivation: The gamma-herpes HHV1 and HHV2 have been found to reactivate with estrogen which seems to support this notion. The beta-herpes CMV has been found to reactivate with estradiol. Estradiol increases the expression of both progesterone and estrogen receptors.

The Flaviviruses may bind the melanocortin receptors. Addition of melanin had a protective effect against the semliki forest virus and the west nile virus slowing the infection rate. The flavivirus Hepatitis C which can infect for years has the same diseases associated with it as the genetic Griscelli syndrome like neutropenia, thrombocytopenia, and NK cell dysfunction. Griscelli syndrome is the result of melanosomes, the melanin pigment containing vesicles, failing to move. MCR1 stimulates melanosomes and could be one of the receptors Hepatitis C uses.

What is even more suggestive is if you consider where the other melanocortin receptors exist and where the other flaviviruses are found. MCR5 is on B cells which during dengue infections appears disrupted and could explain why second exposures to the virus are so harsh. MCR2 otherwise known as the ACTH receptor normally binds ACTH the first hormone involved in an embryo's brain growing and we have a flavivirus, ZIKA, which seems to stunt the growth of baby's brains. The drug suramin is known to bind ACTH. Suramin was found to slow ZIKA infection and bind to the virus directly supporting the notion that Zika uses the ACTH receptor. Yellow fever and hepatitis C infect the liver which has MCR4. West nile infects the kidney which may mean it primarily uses MCR3. These associations are suggestive and need to be considered.

Enteroviruses may bind acetylcholine receptors. Since the Rabies virus of the lyssavirus family have already been proven to bind these receptors it is not too farfetched to assume it is possible that the enteroviruses bind them too. Nicotine has been shown to block coxsackie infections suggesting that nicotinic acetylcholine receptors are involved. Prozac which was recently discovered to block acetylcholine receptors has also been found to help D68 paralyzed children. D68 could be using acetylcholine receptors to infect the nerves. Further note that the toxin curare which binds acetylcholine receptors was used in the treatment of polio. The direct binding of enteroviruses to acetylcholine receptors needs to be proven. Since there are two types of receptors, the muscarinic and the nicotine acetylcholine receptors, the enterovirus family could possibly also be divided into two groups.

Conclusion:

The hypothesis " Virus families use receptor families" is suggestive but more data needs to be collected to validate these receptor-virus matches. Furthermore, this hypothesis should be applied to other virus families such as flu viruses with dopamine receptors, reoviruses with beta-adrenergic receptors, and retroviruses with the albumin binding receptors like the luteinizing hormone receptor.

1. Lentz TL, Burrage TG, Smith AL, Crick J, Tignor GH. Is the acetylcholine receptor a rabies virus receptor? Science. 1982;215(4529):182-184.

2. Low JA, Magnuson B, Tsai B, Imperiale MJ. Identification of gangliosides GD1b and GT1b as receptors for BK virus. J Virol. 2006;80(3):1361-1366. doi:10.1128/JVI.80.3.1361-1366.2006.

3. Tsai B, Gilbert JM, Stehle T, Lencer W, Benjamin TL, Rapoport TA. Gangliosides are receptors for murine polyoma virus and SV40. EMBO J. 2003;22(17):4346-4355. doi:10.1093/emboj/cdg439.

4. Elphick GF, Querbes W, Jordan JA, et al. The human polyomavirus, JCV, uses serotonin receptors to infect cells. Science. 2004;306(5700):1380-1383. doi:10.1126/science.1103492.

5. Assetta B, Maginnis MS, Gracia Ahufinger I, et al. 5-HT2 receptors facilitate JC polyomavirus entry. J Virol. 2013;87(24):13490-13498. doi:10.1128/JVI.02252-13.

6. Yagaloff KA, Lozano G, van Dyke T, Levine AJ, Hartig PR. Serotonin 5-HT1C receptors are expressed at high density on choroid plexus tumors from transgenic mice. Brain Res. 1986;385(2):389-394.

7. Shea PR, (unpublished 2002 ) Identification and Functional characterization of estrogen responsive elements in the human herpesvirus 8 genome

http://d-scholarship.pitt.edu/8097/

8. Offord EA, Leake RE, Macnab JC. Stimulation of estrogen receptor mRNA levels in MCF-7 cells by herpes simplex virus infection. J Virol. 1989;63(5):2388-2391.

9. Kleinman D, Sarov I, Insler V. Reactivation of cytomegalovirus in endometrial cells by estradiol. Gynecol Obstet Invest. 1986;21(3):136-143.

10. Vicetti Miguel RD, Sheridan BS, Harvey SAK, Schreiner RS, Hendricks RL, Cherpes TL. 17-beta estradiol promotion of herpes simplex virus type 1 reactivation is estrogen receptor dependent. J Virol. 2010;84(1):565-572. doi:10.1128/JVI.01374-09.

11. Ing NH, Tornesi MB. Estradiol up-regulates estrogen receptor and progesterone receptor gene expression in specific ovine uterine cells. Biol Reprod. 1997;56(5):1205-1215.

12. Bonilla E, Valero N, Chacín-Bonilla L, Medina-Leendertz S. Melatonin and viral infections. J Pineal Res. 2004;36(2):73-79.

13. Dahal S, Upadhyay S, Banjade R, Dhakal P, Khanal N, Bhatt VR. Thrombocytopenia in Patients with Chronic Hepatitis C Virus Infection. Mediterr J Hematol Infect Dis. 2017;9(1):e2017019. doi:10.4084/MJHID.2017.019.

14. The prevalence and co-occurrence of hematological complications at the time of diagnosis of chronic hepatitis C in Poland: a cross-sectional study. 2016;28(9):1008-1013. doi:10.1097/MEG.0000000000000667.

15. Natural killer cells in hepatitis C virus infection: from innate immunity to adaptive immunity. 2005;3(10 Suppl 2):S78-S81.

16. Different NK cell-activating receptors preferentially recruit Rab27a or Munc13-4 to perforin-containing granules for cytotoxicity. 2009;114(19):4117-4127. doi:10.1182/blood-2009-06-225359.

17. Griscelli syndrome without hemophagocytosis in an eleven-year-old girl: expanding the phenotypic spectrum of Rab27A mutations in humans. 2003;116A(4):329-333. doi:10.1002/ajmg.a.10836.

18. In vitro induction of CD25+ CD4+ regulatory T cells by the neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH). 2001;79(4):358-367. doi:10.1046/j.1440-1711.2001.01022.x.

19. Dose-dependent protective effect of nicotine in a murine model of viral myocarditis induced by coxsackievirus B3. 2015;5(1):2073. doi:10.1038/srep15895.

20. Blockage of muscle and neuronal nicotinic acetylcholine receptors by fluoxetine (Prozac). 1997;94(5):2041-2044.

21. Rationale for the evaluation of fluoxetine in the treatment of enterovirus D68-associated acute flaccid myelitis. 2015;72(5):493-494. doi:10.1001/jamaneurol.2014.4625.

Monday, June 5, 2017

Miller-fisher is a subtype of Guillian Barre. How can Zika virus and TNF alpha trigger ?

Autoimmune cross-targeting is triggered when an infection exists simultaneously on the inside and the outside of a cell causing the immune system attacks the entire cell.

Guillian barre is the peripheral nerves. Miller Fisher seems to have a larger nerve group including the peripheral nerves. Miller-fisher seems to include the lower paralysis or numbness of Guillian barre but then has additional symptoms of double vision, swallowing issues, and ataxia.

Cross-targeting infections:

C.jejune or P. multocida outside
Zika or other flavivirus inside (or for regular Guillian barre CMV)

infection P. multocida and miller-fisher
http://jnnp.bmj.com/content/75/12/1786

infection C. jejune and miller-fisher
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC174172/

Zika and miller-fisher
http://www.neurology.org/content/87/3/336.full
http://journal.frontiersin.org/article/10.3389/fneur.2016.00170/full
http://www.nejm.org/doi/full/10.1056/NEJMoa1605564#t=article
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5044512/

Chikunguny virus (relative of Zika)
https://www.ncbi.nlm.nih.gov/pubmed/28397145
https://www.ncbi.nlm.nih.gov/pubmed/28741102

Chikunguny also infects the brain like zika
http://www.cbc.ca/news/health/chikungunya-brain-infection-1.3337962
http://jcm.asm.org/content/52/9/3459.full

Chikunguny causes microcephaly and cerebral palsy
https://www.ncbi.nlm.nih.gov/pubmed/25033077

melatonin protects against these viruses
http://www.ncbi.nlm.nih.gov/pubmed/14962057

Chikunguny and zika may bind ACTH receptors (chikunguny with less affinity?)

Hepatitis E (a relative of rubella which infects nerves might also trigger miller fisher ?
http://www.readcube.com/articles/10.1007/s10072-016-2644-4

Regular Guillian barre and CMV
https://www.ncbi.nlm.nih.gov/pubmed/28523231
https://www.ncbi.nlm.nih.gov/pubmed/10084538
https://www.ncbi.nlm.nih.gov/pubmed/21214559

Now considering the drugs that trigger the disease. They must replace one of the infections.

TNF alpha antagonist drug causing miller-fisher like issue
https://www.ncbi.nlm.nih.gov/pubmed/16645971
https://www.ncbi.nlm.nih.gov/pubmed/9668366
https://www.ncbi.nlm.nih.gov/pubmed/10511801

What is the normal function of TNF alpha ? To signal that a macrophage has become infected thus stimulating transcription changes. Since this action requires going into the cell the drug likely replaces the virus in the autoimmune cross-targeting scenario.

Does TNF alpha bind the same nerves as Zika?

Zika and chikunguny looks as if it is binding ACTH receptors.

TNF alpha looks as if it is using a different receptor but does seem involved with nerves. (a responsibility beyond macrophage infection)

TNF alpha acts on the TNF1 receptor causing ACTH inhibition
https://www.ncbi.nlm.nih.gov/pubmed/22040432

Paper looking at nerves and TNF alpha contemplating it's involvement there
https://www.hindawi.com/journals/mi/2014/861231/

TNF alpha antagonist and demyelination
https://www.ncbi.nlm.nih.gov/pubmed/19109035

Sorting through other papers looking for more evidence they bind the same nerves

TNF alpha inhibits ACTH ?
https://www.ncbi.nlm.nih.gov/pubmed/2542010
https://www.ncbi.nlm.nih.gov/pubmed/2163305
https://www.ncbi.nlm.nih.gov/pubmed/1702707

Hypotheses: Autoimmune Cross-targeting, Co-carcinogenesis, and Quorum complications