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

Thursday, August 24, 2017

Are Dopamine receptors used by flu viruses and strep ?

Does strep attach using dopamine receptors????

parkinson's symptoms and strep ?
http://www.sciencedirect.com/science/article/pii/S0022347603003664

sydenham's chorea and strep
http://www.uptodate.com/contents/sydenham-chorea

strep and antibodies against dopamine receptors
https://www.ncbi.nlm.nih.gov/pubmed/26454143
https://www.ncbi.nlm.nih.gov/pubmed/24184556
https://www.ncbi.nlm.nih.gov/pubmed/24073196

strep and swollen pancreas
https://pdfs.semanticscholar.org/9b74/24c140687012a49e2dd7ed37d31a6363b1a0.pdf

choline binding proteins of strep A
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC127640/
https://academic.oup.com/jid/article/186/9/1253/940787/Choline-Binding-Protein-A-of-Streptococcus

How does choline connect with dopamine receptors? Choline is known to increase the amount of dopamine receptors and...

choline antagonizes the dopamine receptors directly
https://www.ncbi.nlm.nih.gov/pubmed/7253343

so strep may bind to the dopamine receptors using the choline

Does the flu virus use the dopamine receptors????

the flu virus has a high affinity for dopaminergic neurons
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519479/

Parkinson's symptoms and the flu
https://www.ncbi.nlm.nih.gov/pubmed/21668692

the flu and the pancreas
https://www.ncbi.nlm.nih.gov/pubmed/22361440

my previous post of dopamine receptors and A, B & C flu viruses
http://angelabiggs.blogspot.com/2016/08/5-types-of-dopamine-receptors-and-how.html

choline and the flu viruses' envelope
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4593503/

Friday, August 18, 2017

How do Herpes viruses enter into cells do they use the estrogen receptors or the Herpes-entry-mediator?

Viruses are extremely savvy. Some viruses have evolved to bind the TAM hands of macrophages to block the destruction of virally infected cells. (Macrophages are the immune system's vacuum)

The "herpesvirus entry mediator" is a TNF receptor. This is not the primary mode of entry of the virus rather an attempt to block the immune response.

TNF alpha is released by macrophages when they are themselves infected. (and unable to function) By blocking the receptors for TNF the viruses are trying to "block" the knowledge that macrophages are infected and stop the activation of neutrophils etc.

Neutrophils are the strongest defense of the intestine
https://www.ncbi.nlm.nih.gov/pubmed/22491176

Neutrophils do not have transcription or translation abilities and can therefore deal with viral infections better than macrophages.

Herpesvirus entry mediator
https://link.springer.com/article/10.1245%2Fs10434-017-5924-1

this TNF receptor has high levels in the mucosal membranes
https://www.ncbi.nlm.nih.gov/pubmed/24851095

I still contest that the main mode of Herpes viral entry on regular cells is through estrogen receptors.

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

Estrogen-related receptors and estrogen-alpha receptors cycle to the nucleus which is why these herpes viruses can cause cancer while the Beta-estrogen receptors cycle to the mitochondria where alpha herpes viruses can hide for years.

Wednesday, August 16, 2017

Suramin, Zika virus, and the ACTH receptor

The Zika virus looks as if it binds the ACTH receptor.

I have been dividing up the flaviviruses with the melanocortin receptor they could use:

mcr1 Tick borne encephalitis virus/ hepatitis C (Thrombocytopenia due to red blood cells with mcr1)

mcr2 (ACTH receptor) Zika (placenta, developing brain)

mcr3 West nile (kidneys)

mcr3 and mcr1 Japanese encephalitis

mcr4 Yellow fever (liver)/ hepatitis C

mcr5 Dengue (immune system T cells)

Previous posts of Zika and ACTH receptors
http://angelabiggs.blogspot.com/2017/07/zika-malaria-drugs-and-acth-receptor.html

Suramin blocks Zika infection by binding were the virus attaches
https://www.ncbi.nlm.nih.gov/pubmed/28457855
https://www.ncbi.nlm.nih.gov/pubmed/28461070

Suramin binds the ACTH molecule
https://www.ncbi.nlm.nih.gov/pubmed/2152879

So is suramin binding the virus as if it is an ACTH molecule? Does this support the hypothesis that Zika uses ACTH receptors?

note that suramin is a drug that kills parasites and is used against the sleeping sickness and has been found to find to do other actions....but here with Zika it interferes with viral attachment

Previous post linking virus families to receptor families
http://angelabiggs.blogspot.com/2017/06/updated-virus-families-bind-and-enter.html

The Immune system pathways in terms of infections on the outside of host cells

Imagine macrophages as the vacuums of the immune system carrying TLRs like butterfly nets trying to identify foreign material on bacteria it needs to consume.

In addition to these "nets" macrophages also look for opsonins. Opsonins are grab handles your immune system puts on infections for macrophages.

Here are how opsonins are placed on infections:

Most gram positive bacterias have thick peptidoglycan cells which antibodies bind easily. (staph for example has a very flat surface) When two antibodies are in close proximity the classical pathway is triggered where opsonins are latched on to the surface of the bacteria. Remember to think of opsonins as macrophage grab handles. (C4b and C3b are opsonins)

The use of antibodies is called the classical pathway.

However some infections like strep have added a layer of lipopolysaccharides to make it more difficult for two antibodies to touch. Your immune system has developed a sugar binding pathway called the lectin pathway using a mannose binding protein. This mannose binding protein, MBP, binds the sugar and triggers the opsonins. (instead of 2 antibodies)

Lectin pathway and strep
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4300866/

Lectin and candida
https://www.ncbi.nlm.nih.gov/pubmed/26730718

Lectin pathway and spirochetes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170916/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179856/

Now imagine a gram negative bacteria like e.coli. Gram negative bacterias have evolved a very thin peptidoglycan layer with a crazy thick camouflage layer of varying stuff. E.coli for example is covered with pili. The surface of the bacteria is not easily visible or accessible to a macrophage and therefore the opsonins grab handles won't be easily used.

Image of e.coli

http://visualsunlimited.photoshelter.com/gallery-image/E-coli/G0000t5nqL4ZyAkU/I0000kKu0VV1fZb0/C0000.oQ5ArSj2dQ

It is in these circumstances that the opsonins collecting on the surface form C5 and go on to bind with C8 and C9 to form the MAC, the membrane attack complex. The MAC is literally a pore created by your immune system on the bacteria's membrane with purpose of leaking the guts of the bacteria out.

The alternative pathway would best be described as a short cut path. If the opsonins are struggling to build up on the surface and remain free floating they can still become the C5 free floating and then attach to the surface...short cutting the path to the MAC pore.

Friday, August 11, 2017

Can zika bind melanocortin4 receptor to some degree causing the damage to the liver and heart? Assuming zika binds the ACTH receptors( mcr2)

melanocortin 4 receptor, obesity, and heart rate
https://www.ncbi.nlm.nih.gov/pubmed/25668357

same article but full paper...over activation of MCR4 lowers heart rate
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4748968/

capsaicin
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477151/

https://www.news-medical.net/news/20150423/Capsaicin-has-beneficial-effects-on-liver-damage-study-reveals.aspx

melanocortin 4 receptor malfunction and high cholesterol
https://www.ncbi.nlm.nih.gov/pubmed/28030540

Zika takes 81 days to leave system
http://www.empr.com/news/zika-virus-infections-semen-saliva-vaginal-cdc-mosquito/article/638351/

Zika uses melanocortin receptor 2....the ACTH receptor

Does this mean that the Zika can trigger some MCR4?

MCR4 can bind ACTH
https://www.ncbi.nlm.nih.gov/pubmed/24085819

Zika and the heart
http://www.acc.org/about-acc/press-releases/2017/03/09/13/25/researchers-sound-alarm-over-zikas-potentially-harmful-heart-effects

zika and the liver

http://hrjournal.net/article/view/1589

Yellow fever and heart rate
http://www.nytimes.com/health/guides/disease/yellow-fever/overview.html

I had previously predicted that the yellow fever virus used the MCR4.
http://angelabiggs.blogspot.com/2017/05/flaviviruses-melanocortin-receptors-and.html

Friday, August 4, 2017

The spirochetes: Lyme: Borrelia, Syphilis: Treponema, and Leptospira all cause high cortisone disorders and clotting disorders

Spirochetes could be disturbing the cortisone levels causing cataracts, depression, anxiety and hoarding.

http://angelabiggs.blogspot.com/2016/04/anterior-cingulate-cortex-hoarding.html

Spirochetes also appear to cause bleeding/clotting disorders: how ?

Thrombocytopenia or severe clotting with Leptospira
http://www.ncbi.nlm.nih.gov/pubmed/7044515
https://www.ncbi.nlm.nih.gov/pubmed/16451735
https://www.ncbi.nlm.nih.gov/pubmed/18171258
https://www.ncbi.nlm.nih.gov/pubmed/9080878

why ? because leptospira binds the prothrombinase and triggers clotting
https://www.ncbi.nlm.nih.gov/pubmed/28400758

Syphilis' Treponoma also distrupts clots
https://www.ncbi.nlm.nih.gov/pubmed/24303899

spirochetes bind laminin?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153296/

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