Could the Dengue virus' second exposure be worse because of the types of white blood cells it infected? A lack of T cells

Could the Dengue virus' second exposure be worse because of the types of white blood cells it infected the first time? Could the white blood cells with melanocortin receptors be missing from the second response?

Second response to Dengue is dominated by reactive plasmablasts
http://www.ncbi.nlm.nih.gov/m/pubmed/27030262/
http://jvi.asm.org/content/86/6/2911.full

there is an association between the size of the plasmablast response and the severity of disease of the second response
http://www.jimmunol.org/content/190/1/80.abstract 

Memory B cells transition to plasmablasts then into plasma cells. As they do so the level of antibody secretion increases
http://www.ncbi.nlm.nih.gov/m/pubmed/27030262/

What happened to the T cells? I believe that Dengue uses the MCR5 receptor

Melanocortin 5 receptors are involved in inflammation at the spleen by the T cells
https://www.ncbi.nlm.nih.gov/pubmed/24043903
https://www.ncbi.nlm.nih.gov/pubmed/21989727

 "Primed T cells express the melanocortin 5 receptor (MC5r)"
http://www.ncbi.nlm.nih.gov/pubmed/11488983

Imagine the second exposure to dengue viruses as chaotic in that the awakened memory B cells are labeling everything but the Dengue virus has infected and destroyed most of the T cells ( through MCR5).

There are 4 types of Dengue and the severe reaction is typically when the second exposure is with a different dengue (that the antibodies do not recognize?)
http://www.ncbi.nlm.nih.gov/m/pubmed/21219187/?i=6&from=/27030262/related

Below are the reasons I think the flaviviruses are using the melanocortin receptors:

Melatonin protects from a flavivirus infection
http://www.ncbi.nlm.nih.gov/pubmed/14962057

Kidney cells have MCR1, MCR3, and 4. Embryonic cells have MCR5. Brain was the only one with MCR2.
http://www.sciencemag.org/news/2016/03/zika-virus-kills-developing-brain-cells

Zika is probably using MCR2 (ACTH receptor) while Dengue would be using MCR5.  Note that ACTH is the first hormone used for brain development and zika has been found infecting the fetal brain.

In general, embryonic cells would be infected by the Dengue because they express MCR5.

Embryonic heart cell and dengue
http://www.ncbi.nlm.nih.gov/pubmed/25598317

Dengue vaccines and the mcr-5 cell line
https://micro.magnet.fsu.edu/primer/techniques/fluorescence/gallery/cells/mrc5/mrc5cells.html

Thyroid issues, melantonin, and dengue

melatonin increases/stimulates the thyroid...by stimulating a melanocortin receptor
http://www.ncbi.nlm.nih.gov/pubmed/11083464

dengue and subacute thyroiditis...is this the same thing?? but dengue is triggering the receptor of the thyroid instead of melatonin
http://www.ncbi.nlm.nih.gov/pubmed/23033818

or has melatonin itself been released (by the immune system) in an attempt to call inflammation and  awaken T cells
previously melatonin had been found to be released as an anti-inflammatory agent by the immune system
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645767/
http://www.ncbi.nlm.nih.gov/pubmed/23827742
http://www.ncbi.nlm.nih.gov/pubmed/9218248 (melanocortins modulate fever)

Subacute cutaneous lupus erythematosus, Aspergillus fumigatus, and gliotoxins

Subacute cutaneous lupus erythematosus and aspergillus fumigatus
http://www.ncbi.nlm.nih.gov/pubmed/18374855
http://www.ncbi.nlm.nih.gov/pubmed/7894223 (pneumonia)

lupus and aspergillus fumigatus with increased granulocytopenia
http://www.ncbi.nlm.nih.gov/pubmed/7604298

Granulocytopenia (a type of white blood cells )
https://en.wikipedia.org/wiki/Granulocyte#Pathology

Does the toxin that aspergillus secretes cause this condition of granulocytopenia in lupus?

Aspergillus fumigatus secretes gliotoxin ab immune suppressing toxin
http://www.ncbi.nlm.nih.gov/pubmed/17574915
http://www.bloodjournal.org/content/105/6/2258?sso-checked=true
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2708386/

some lupus has sun sensitivity
http://emedicine.medscape.com/article/1065657-overview

Gliotoxin inhibits Farnesyltransferase
https://link.springer.com/article/10.1385/MO:21:1:21

Rash and inhibition of farnesyltransferase
http://onlinelibrary.wiley.com/store/10.1002/cncr.23078/asset/23078_ftp.pdf?v=1&t=jeu2bcuc&s=874bb318f5b62fb928cc2d0fa7942c375de01181

How does the rash occur?? Is it gliotoxin directly broken down or gliotoxins's inhibition of Farnesyltransferase ?

note that gliotoxin contains a disulfide bridge
http://www.ncbi.nlm.nih.gov/pubmed/15584558

sun exposure damages disulfide bridges
http://marketplace.yet2.com/app/insight/needofweek/6244?sid=350

CNS lupus, neuropenia, and cryptococcus neuformans are linked by copper

CNS lupus
http://www.ncbi.nlm.nih.gov/pubmed/1866569

Cryptococcus neoformans... lupus with menegitis
http://rheumatology.oxfordjournals.org/content/46/3/539.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2496186/pdf/postmedj00297-0075.pdf
http://onlinelibrary.wiley.com/doi/10.1046/j.1439-0507.2001.00661.x/abstract

copper and cryptococcus requires a ton of it
http://www.nature.com/ncomms/2014/141124/ncomms6550/abs/ncomms6550.html

Nerves and copper
http://www.ncbi.nlm.nih.gov/pubmed/8456123

copper and the human brain
http://www.ncbi.nlm.nih.gov/pubmed/6521817

pulminary lupus and cryptococcus infection
http://www.ncbi.nlm.nih.gov/pubmed/8493585

myocytes (heart cells) could be considered nerves crossed with muscles

Heart rate requires copper
http://www.sciencedirect.com/science/article/pii/0025326X87905741

copper deficiency can cause neuropenia
https://en.wikipedia.org/wiki/Copper_deficiency

neutropenia in lupus
http://rheumatology.oxfordjournals.org/content/45/8/994.full.pdf

neutropenia (lower levels of neutrophils)
https://en.wikipedia.org/wiki/Neutropenia

Pernio/ chilbain, Raynoids, SLE, sarcoidosis: Is the fungus Aspergillus parasiticus involved?

The autoimmune hypothesis of this blog suggests that it is the cross-targeting of infections on one tissue that triggers autoimmune disease.  In the case of lupus the larger outer infection could be a type of aspergillus fungus.

lupus and aspergillus
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3768502/
http://www.ncbi.nlm.nih.gov/pubmed/8720197
http://www.ncbi.nlm.nih.gov/pubmed/12090570
http://www.ncbi.nlm.nih.gov/pubmed/12412216
http://www.ncbi.nlm.nih.gov/pubmed/8989808
http://www.ncbi.nlm.nih.gov/pubmed/9352608

multisystem sarcoidosis and aspergillus
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116216/

Scotland has high levels of Pernio
The most common aspergillus in Scotland is A. parasiticus (61%)
http://www.ncbi.nlm.nih.gov/pubmed/23416649

This is a hypothesis that A.parasiticus specifically causes pernio.

Chilblain aka pernio
https://en.wikipedia.org/wiki/Chilblains
http://www.ncbi.nlm.nih.gov/pubmed/2212122

appears to overlap with sarcoidosis
http://www.ncbi.nlm.nih.gov/pubmed/27222775

lupus pernio from infliximab
http://www.ncbi.nlm.nih.gov/pubmed/26147319

infliximab /Remacade  : drug used against TNF-alpha in autoimmune diseases
https://en.wikipedia.org/wiki/Infliximab

Aspirin and TNF-alpha
http://www.ncbi.nlm.nih.gov/pubmed/15036249

high TNF-alpha is involved with sarcoidosis
http://www.ncbi.nlm.nih.gov/pubmed/14746631

mixed connective tissue disease: SLE with Scleroderma and polymyositis
http://rarediseases.org/rare-diseases/mixed-connective-tissue-disease-mctd/

Lupus can be triggered by TNF-alpha inhibitors!

lupus/neck pain with the butterfly rash across face: tiny blood vessels
http://www.lupusresearch.org/lupus/symptoms.html?referrer=https://www.google.com/#.V4uG6JOAOkp

What causes this contraction of the blood vessels?

Quorums are the communication molecules infections use.

What are Aspergillus' quorums: ACTH? tyrosol? A. niger also has aflatoxin.

ACTH would disrupt the adrenal glands

aspergillus and ACTH
http://www.ncbi.nlm.nih.gov/pubmed/23967728

addison's disease and SLE (uncommon but there)
http://www.ncbi.nlm.nih.gov/pubmed/25400892
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3952287/
http://www.ncbi.nlm.nih.gov/pubmed/9228146

adrenal involvement in anti-phospholipid syndrome
http://www.ncbi.nlm.nih.gov/pubmed/12640187

Lupus and anti-phospholipid syndrome
http://jasn.asnjournals.org/content/18/9/2461.full

Previous blog linked addison's and the fungus candida together through farsenol
http://angelabiggs.blogspot.com/2015/12/candidas-quorum-sensing-and-addisons.html

The quorum tyrosol would cause pigment issues (if secreted by aspergillus) and could also cause the blood vessel contraction/ dilation

Chilblains is a blood circulation issue where damage occurs to blood vessels due to cold.

Normally cold exposure cases vasoconstriction where blood is pulled away from skin. Warm exposure then triggers Vasculitis where the blood vessels expand.

An excessive amount of tyrosol inducing dilation of vessels could prevent the normal vasoconstriction during exposure to cold. Thus the hands or feet would look purple and swell.

Chilblian lupus and discord lupus overlap
https://www.derm101.com/dpc-archive/january-march-1999-volume-5-no-1/dpc0501a20-pernio-perniosis-lupus-pernio-chilblain-chilblain-lupus/

Previous post about a different fungus Trichophyton and tyrosol (discord lupus)
http://angelabiggs.blogspot.com/2016/02/tyrosol-as-quorum-of-trichophyton.html

The difference here is where the fungus hangs out: trichophyton infects the skin where as aspergillus parasiticus infects inside the body often the lungs

tyrosol from Aspergillus in soy

https://books.google.com/books?id=-M5t2nXIXi4C&pg=PA636&lpg=PA636&dq=tyrosol+vessels&source=bl&ots=7IxkWckjs8&sig=F9mu2_o7oSUR5qOnXxKETTPoM48&hl=en&sa=X&ved=0ahUKEwj0sa203PrNAhVqzoMKHXsDC_sQ6AEITTAJ#v=onepage&q=tyrosol%20vessels&f=false

Do the forms of lupus that occur in japan have a distinctive pigment issue? or are we seeing that these fungus prefer to grow in different locations: aspergillus inside the body while trichophyton prefers the skin

Aflotoxin from A.niger I had been looking at as a trigger for Pick's dieseases Tau protein

lupus and pick's disease

http://www.ncbi.nlm.nih.gov/pubmed/25966928

Are cancer tumors killing Australia's green turtles?

Co-carcinogenesis Hypothesis: A virus and carcinogen together cause cancer

Cancer occurs because a carcinogen inhibits the viral polymerase better than the human polymerase. When a virus infects the same cell as a carcinogen they interact.  Instead of the virus making what it wants in the host the infected cell is transformed into a cancer cell by the carcinogen. 

Previously I suggested that herpes viruses and benzene both use estrogen receptors to enter cells therefore they tend to cause cancer together
http://angelabiggs.blogspot.com/2016/06/cancer-and-receptors.html

Estrogen receptors and benzene references
http://angelabiggs.blogspot.com/2016/06/benzene-carcinogen-binds-estrogen.html

Great barrier reef oil spill
https://en.wikipedia.org/wiki/2010_Great_Barrier_Reef_oil_spill

Benzene in the turtles' sea grass

https://books.google.com/books?id=NRPXN7T2YdUC&pg=PA314&lpg=PA314&dq=green+turtles+benzene&source=bl&ots=YQKbLN55FK&sig=YXrKr3tzwhl9YNeUKeYzSBzcgy8&hl=en&sa=X&ved=0ahUKEwj6-fb3-vXNAhUX2WMKHUq5Bj4Q6AEITDAG#v=onepage&q=green%20turtles%20benzene&f=false

Fibropapillomatosis are the turtle tumors caused by the herpes virus. They say the tumors are benign not cancerous...but why do the tumors only form on some turtles when more are infected?
https://en.wikipedia.org/wiki/Fibropapillomatosis

Do the turtles with tumors have Benzene from the oil spill in 2010?

Zika virus, Green Tea, Agouti-related peptides, and the ACTH receptor

Green tea and Zika
http://www.contagionlive.com/news/study-reveals-how-green-tea-could-protect-against-zika-virus

What could be happening here is that the agouti-related proteins are competing with the Zika virus for the ACTH receptors.

Zika and ACTH (hypothesis of a previous blog posts)
http://angelabiggs.blogspot.com/2016/01/does-zika-virus-use-melanocortin.html

Gaba and melanocortin system in the hypothalamus
http://www.nature.com/nrendo/journal/v10/n11/fig_tab/nrendo.2014.160_F1.html
This shows how the neuron releases GABA and Agouti-R together but act on different receptors.

EGCG (green tea) and the hippocampus neurogenesis
http://onlinelibrary.wiley.com/doi/10.1002/mnfr.201200035/abstract
Is this the Agouti-R acting on melanocortin receptors in this case?

Green tea increases serotonin which increases the release of GABA and Agouti-related peptide
http://healthyeating.sfgate.com/can-green-tea-boost-serotonin-3386.html

Agouti-relate peptide
https://en.wikipedia.org/wiki/Agouti-related_peptide
Is made and released with GABA in the hypothalamus only Agouti-R acts on the melanocortin 3 and 2 receptors not the GABA receptor

ACTH is the Melanocortin 2 receptor which is responsible for neurogenesis

Spirochetes and high cortisol

How do spirochetes increase cortisol levels? do they secrete cortisol or is it the endotoxin they secrete that raises the levels?

Lyme's bacteria releases an endotoxin with zinc endopeptidase properties..similar to tetanus?
http://www.ncbi.nlm.nih.gov/pubmed/7925446

Tetanus's zinc-endotoxin causes the inhibition of acetylcholine release (the paralysis)
http://www.ncbi.nlm.nih.gov/pubmed/1396558

acetylcholine causes cortisol secretion
http://www.sciencedirect.com/science/article/pii/030372079090147Z

Is the body countering these inhibitors and increasing acetylcholine release?

paralysis from lyme has occurred but is not common
https://www.sciencedaily.com/releases/2000/01/000113080050.htm

maybe lyme's chronic nerve pain is actually over stimulation instead of
inhibition?

previous post : spirochetes may attach where Vit C does in the body
http://angelabiggs.blogspot.com/2016/06/does-hpylori-bind-to-sodium.html

previous post : spirochetes, poison ivy allergies, and cortisol levels (cataracts, depression)
http://angelabiggs.blogspot.com/2016/05/severe-poison-ivy-reactions-and.html

Paradigm shifts in Cancer and Autoimmune disease are about to occur

A scientific paradigm shift occurs when current assumptions are suddenly realized to be either wrong or "off" enough that when a new hypothesis appears based on different assumptions that when tested explains more, predicts more, and thus creates a fundamental shift in the field.

Cancer's paradigm shift

Lately the assumption in cancer has been that DNA damage causes cancer however patterns exist that favor Francis Peyton Rous' older hypothesis that "co-carcinogenesis" causes cancer.  We now know there are cancers that seem to appear together, prostate and skin cancer, if that is a true relationship how can it be random DNA damage?  Rous believed a carcinogen and a virus together causes cancer not DNA damage and conducted the first experiments to prove this.

My co-carcinogenesis hypothesis 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. All carcinogens have already been found to inhibit polymerases.  Further it is already known which cell types the carcinogens infect. 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's telomeres to create virus supplies forever.  This inhibiting of growth is what we see with too much carcinogens for example too much benzene in bone marrow and the person becomes anemic.  

Cancer occurs because a carcinogen inhibits the viral polymerase better than the human polymerase. When a virus infects the same cell as a carcinogen they interact.  Instead of the virus making what it wants in the host the infected cell is transformed into a cancer cell by the carcinogen. 

Autoimmune Diseases' paradigm shift

Currently it is believed that autoimmune diseases are chaotic and slowly developed.  As if the immune system slowly becomes crazy through inflammation and genetic defect.  However patterns exist that suggest quite the opposite that autoimmune disease is triggered suddenly and most importantly is a predictable occurrence. 

If you look at the Autoimmune diseases that occur together and look for a shared infection you find areas of overlap. Sjogren's, Hoshimoto's thyroid, and type one diabetes have all been linked to fungal infections.

 However different infections can trigger the same disease: coxsackie or the flu can trigger type 1 diabetes which seems to say the specific infection is not important and it is an immune system dysfunction that is critical.

So here is the paradigm shift: the infections exist for a while in the host but the infections themselves to not slowly lead up to the autoimmune disease rather the immediate dysfunction of the immune system faced with "autoimmune cross-targeting" triggers autoimmune disease.

Autoimmune cross-targeting hypothesis suggests that simultaneous infections on one target triggers autoimmunity.  One infection on the outside of the target cell and one infection, like a virus, on the inside of the target.   Note that chemicals and drugs can replace an infection as foreign to the immune system.

This blog has been going through the cancers and autoimmune diseases testing these hypotheses and I am at the point now where I can say....prepare yourself for HUGE paradigm shifts.  

Happy 4th of July! Let's have a huge boom today...please share this!

Do retroviruses use the thrombopoietin receptors?

Chronic myeloid leukemia and HIV?  rare?
http://www.ncbi.nlm.nih.gov/pubmed/22527850
http://www.ncbi.nlm.nih.gov/pubmed/22867899
http://www.ncbi.nlm.nih.gov/pubmed/18452074

Thrombopoietin receptors and CML Chronic myeloid leukemia
http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-0142(20000201)88:3%3C570::AID-CNCR12%3E3.0.CO;2-I/full

Thrombopoietin receptors and HIV infections?

Thrombocytopenia in HIV
http://www.ncbi.nlm.nih.gov/pubmed/16454716
http://www.ncbi.nlm.nih.gov/pubmed/9616135

liver and HIV
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997131/

Kidney and HIV
http://hivinsite.ucsf.edu/InSite?page=kb-00&doc=kb-04-01-10

TPO
http://www.bloodjournal.org/content/98/12/3241?sso-checked=true

Thrombopoietin is made by liver, kidney, and bone marrow cells..all of which we see infected by HIV


what about other retroviruses? do they infect the same type of cells?

rous sarcoma virus and kidney cells
http://www.ncbi.nlm.nih.gov/pubmed/3015940

rous sarcoma virus and liver cells
http://www.ncbi.nlm.nih.gov/pubmed/2177729

Further note that 70% of people with HIV have sleep issues
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543776/

Thrombopoietin production is controlled  by the circadian sleep/wake cycle
http://onlinelibrary.wiley.com/doi/10.1111/j.1538-7836.2012.04643.x/abstract

mplv, a retrovirus, has been linked to the thrombopoietin receptor by the thrombopoietin-like protein it makes

https://books.google.com/books?id=bfPORhG6DP8C&pg=PT139&lpg=PT139&dq=htlv+retrovirus+Thrombopoietin&source=bl&ots=bUDYfErtXg&sig=v5KvUb0mtaFqeQUPuUz_rCaAKVE&hl=en&sa=X&ved=0ahUKEwibjMH7hNPNAhVB8GMKHSl-AtMQ6AEIaTAJ#v=onepage&q=htlv%20retrovirus%20Thrombopoietin&f=false

why would the virus make this protein? Is this how it binds the receptors?

The 4 types of leukemia, the associated viruses, and co-carcinogenesis

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 to create virus supplies for ever.  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.

There are 4 types of leukemia and they are associated with different viruses

Acute myeloid leukemia AML and flaviviruses

AML and dengue virus

http://www.ncbi.nlm.nih.gov/pubmed/11524267

west nile and leukemia
http://www.ncbi.nlm.nih.gov/pubmed/16344671
http://journals.lww.com/jpho-online/Abstract/2005/12000/West_Nile_Virus_Infection_in_a_Teenage_Boy_With.6.aspx
http://wwwnc.cdc.gov/eid/article/7/4/01-7432_article ?
http://www.auntminnie.com/index.aspx?sec=ser&sub=def&pag=dis&ItemID=56900?
Hepatitis C and acute leukemia
http://www.ncbi.nlm.nih.gov/pubmed/8037177

(Flaviviruses might be using melanocortin receptors)

Chronic myeloid leukemia CML and the HIV virus

HIV and CML
http://www.ncbi.nlm.nih.gov/pubmed/18452074
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932605/
http://www.ncbi.nlm.nih.gov/pubmed/11361394
https://www.researchgate.net/publication/224820749_Chronic_myeloid_leukaemia_and_human_immunodeficiency_virus_HIV_infection

(HIV is a retrovirus and they may use gangliosides )

Acute lymphocyte leukemia ALL and HTLV viruses (involves t-cells)

HTLV-1
http://www.lymphoma.org/atf/cf/%7B0363cdd6-51b5-427b-be48-e6af871acec9%7D/htlv.pdf
http://emedicine.medscape.com/article/219285-overview

HTLV-2 and hairy cell leukemia
http://science.sciencemag.org/content/218/4572/571.long

feline leukemia virus is a retrovirus
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509668/

mice have a version of these: murine leukemia virus
https://en.wikipedia.org/wiki/Murine_leukemia_virus

a new type of murine virus has been suspected of infecting people: xenotrophic murine leukemia virus
http://jid.oxfordjournals.org/content/202/10/1463.full

koalas have leukemia causing retroviruses
https://retrovirology.biomedcentral.com/articles/10.1186/1742-4690-10-108



Chronic lymphocytic leukemia CLL and HPV viruses

lymphocytic leukemia (CLL) and cervical cancer

http://www.ncbi.nlm.nih.gov/pubmed/20506683

CLL and HPV

http://www.ncbi.nlm.nih.gov/pubmed/20230400

(HPV viruses may use the cannabinoid receptors and this group may be the group that cannabinoid, marijuana, helps)