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
HLA-DQ non encapsulated virus in cytosol
HLA-DP antigen presenting cells' HLA


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



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

Viruses, Benzene rings, and disulfide bridges


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

The negative group 

HPV - cannabinoid receptors
Flaviviruses - melanocortin receptors
Flu - dopamine receptors
Herpes viruses - estrogen receptors

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

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

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

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?


Thursday, December 1, 2016

HPV, Lipids, cannabinoid receptors, and HLAs....contemplations

I had previously hypothesized that HPV was using cannabinoid receptors to enter cells: there are two types of cannabinoid receptors CB1 and CB2.

HPV and HLA-C ?

cervical cancer, HPV, and HLA-C
https://www.ncbi.nlm.nih.gov/pubmed/23398510

Which means that lipid binding of the cannabinoid receptor causes it to internalize and go to the endoplasmic recticulum, hence the HLA-C mailbox involvement. (which makes sense because the smooth ER is involved with lipid metabolism)

Cannabinoid receptors and lipids
http://www.bbm1.ucm.es/cannabis/archivos/publicaciones/Life_Sci05_77_1723_1731.pdf

Malignolipids and the cancers connected to HPV viruses: gastric, colon, uterine, and breast cancer

Malignolipids
http://onlinelibrary.wiley.com/doi/10.1002/1097-0142(196608)19:8%3C1149::AID-CNCR2820190816%3E3.0.CO;2-L/full

Does HPV make malignolipids? Is this it's outer coat? Is this what the HPV uses to bind the cannabinoid receptors to enter cells? What exactly are malignolipids?

Note that the major risk HLA for cervical cancer is HLA-dp
https://www.ncbi.nlm.nih.gov/pubmed/26711785
https://www.ncbi.nlm.nih.gov/pubmed/23428460

HLA-DP is the HLA of antigen presenting cells of the immune system

I have connected HLA-DP3 with lipids.
My bet is that it is specifically HLA-DP3 even though these references does not indicate it.