Postural orthostatic tachycardia syndrome (POTS) is it reoviruses or autoimmune cross-targeting? autonomic dysfunction and e.coli?

Is Postural orthostatic tachycardia an autoimmune disease or is it the result of a reovirus alone?

POTS and autoimmunity
http://www.ncbi.nlm.nih.gov/pubmed/24572257

what is reovirus?
https://en.wikipedia.org/wiki/Reoviridae

Reoviruses are non enveloped viruses which cause gastro intestinal issues.

reoviruses can contaminate egg shells
http://www.thepoultrysite.com/publications/6/diseases-of-poultry/200/reovirus-infections/

reovirus can bind adrenergic receptors
http://jvi.asm.org/content/64/2/639.full.pdf
http://www.ncbi.nlm.nih.gov/pubmed/2831655

actually binds the antagonist site of the receptor (blocks it?)
http://jvi.asm.org/content/64/2/639.full.pdf

reoviruses, isoprel, and beta-adrenergic receptors...no shared binding???
http://europepmc.org/abstract/med/2831655

isoprel activates beta adrenergic receptors

Autoantibodies to adrenergic receptors in POTS syndrome
http://www.ncbi.nlm.nih.gov/pubmed/24572257

Gardasil and POTS connection
http://www.ncbi.nlm.nih.gov/pubmed/25882168

Is it the HPV trigger cross-targeting with a larger infection or is it contamination of the vaccine by a reovirus?

Vaccines are made using eggs creating the possibility of egg shell contamination hence the warning of egg allergy and vaccines

Could contamination of the Gardasil vaccine by reoviruses cause the development of POTS?

The safety of Gardasil vaccines and the link to Pots might disappear when the method of vaccine development changes if it is the reovirus
http://allergynotes.blogspot.com/2010/03/next-generation-of-flu-vaccines-cell.html

I say this because I believe in vaccination

note that some cases of POTS have been connected to gastrointestinal issues which could be the group of POTS not connected to vaccines

gastro complaints with POTS patients
http://www.ncbi.nlm.nih.gov/pubmed/24068608

also note that reoviruses can infect fungus
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC368758/

could this explain the overlap of Sjogren's and Hashimoto's with POTS if they are caused by fungal infections?

or is it the fact most yeasts have something like reoviruses in them?
http://www.nature.com/nature/journal/v268/n5619/abs/268464a0.html

or is it the fungus cross-targeting with the HPV?

the reason I changed my mind that POTS was autoimmune, I am leaning toward the reovirus, was my discover that some of the  flu vaccines can cause it....HPV and the flu are very different viruses

http://forums.phoenixrising.me/index.php?threads/our-difficulties-with-current-flu-vaccine-and-dysautonomia.6713/

detection of reovirus in bird flu vaccine
http://www.ncbi.nlm.nih.gov/pubmed/15620400

The adrenergic system involves the use of the neurotransmitters epinephrine and norepinephrine while cholinergic uses acetylcholine

Note that there are 3 types of POTS: neuropathic (idiopathic nerve disease), hyperadrenergic (high nor-epinephrine levels),  secondary (caused by circulation issues like diabetes)

genetic POTS is the nor-ephinephrine type
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600095/

since reoviruses bind adrenergic receptors do they trigger POTS?

Or is it autoimmune cross-targeting which would indicate damage to the heart is occurring. Is this true? does the immune system attack the heart? or is it merely a reovirus infection

Autoimmune cross-targeting hypothesis:  the layering of 2 different infections on one target triggers autoimmune disease.  A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria infection marking the outside.

At this point it seems that the heart is not being attacked by the immune system but rather that somehow the adrenergic receptors are over stimulated. Either by reoviruses or the antibodies seeking the binding of them?

Note that salmonella and e.coli use epinephrine /norepinephrine as their quorums (communication signals between the bacteria
https://www.readbyqxmd.com/read/16487745/quorum-sensing-in-escherichia-coli-and-salmonella

Celiac patients tent to have bladder infections histories and bladder infections are commonly e.coli infections

Could e.coli not only trigger the autoimmune cross-targeting of celiac disease but be the cause of the autonomic dysfunction?

autonomic dysfunction and celiac
http://www.ncbi.nlm.nih.gov/pubmed/25554987
http://www.ncbi.nlm.nih.gov/pubmed/25962148
http://www.ncbi.nlm.nih.gov/pubmed/20940666

note that this is different from the autoimmune attack of the peripheral nerves which is like guillian barre

Campylobacteria/sutterella could probably trigger the celiac and guillian barre but not POTS.

POTS after chicken pox infection (zoster)....and anti-virals?
https://www.researchgate.net/publication/290480129_P-B34_Postural_tachycardia_syndrome_POTS_after_Varicella_Zoster_virus_infection_chicken_pox

anti-viral ribavirin and reovirus
http://www.sciencedirect.com/science/article/pii/0042682289904133

ribavirin and zoster
http://www.ncbi.nlm.nih.gov/pubmed/3298116

ribavirin
https://books.google.com/books?id=aoeBKqsswM8C&pg=PA70&lpg=PA70&dq=ribavirin+yeast&source=bl&ots=WQ6c3tcA0z&sig=eaZrMnYwvkD6jZFO9uYqEoepnlw&hl=en&sa=X&ved=0ahUKEwjqis6T2PDOAhUUHmMKHR46BVo4ChDoAQhWMAk#v=onepage&q=ribavirin%20yeast&f=false

flu and pots
http://forums.phoenixrising.me/index.php?threads/our-difficulties-with-current-flu-vaccine-and-dysautonomia.6713/

http://www.uscfc.uscourts.gov/sites/default/files/opinions/MORAN.HIBBARD052511.pdf

if from reovirus of egg shells

avian reovirus affects joints
http://www.ncbi.nlm.nih.gov/pubmed/2163092
http://www.ncbi.nlm.nih.gov/pubmed/10935283

POTS tends to have hypermobility in joints
http://www.edhs.info/#!dysautonomia-and-edhs/clvf

http://www.dynakids.org/Documents/hypermobility.pdf

hock
http://articles.extension.org/pages/65756/hock

epinephrine is used in local anesthetics to limit bleeding (constricts local blood supply)


some people react to the epinephrine..."pots" people?

Is Sjogren's triggered by autoimmune cross-targeting? So many suspects..can we divide up sjogren's into several types?

Autoimmune cross-targeting hypothesis:  the layering of 2 different infections on one target triggers autoimmune disease.

A viral infection marking the inside of the target then an external infection marking the outside. One of each is needed to trigger autoimmunity.

Sjogren's: autoimmune disease of the salivary glands (target tissue)

external infection suspects that could be marking the outside of the gland:

mycoplasmas with RA associations
fungal with hoshimoto's thyroid
spirochetes with lichen sclerosis

viral internal infection suspects:

EBV/HHV8 (using alpha estrogen receptors)
retroviruses (using thrombopoietin receptors..RANK?)
hepatitis C (using mc1 receptors)
??? HPV16 (using CB1 receptors)????

mycoplasmas and sjogren's
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC477189/

RA and  sjogren's
http://www.medscape.com/viewarticle/808825
http://www.ncbi.nlm.nih.gov/pubmed/2200936

personal post sjogren's and lyme
http://sjogrensvegan.blogspot.com/

estrogen alpha receptor is involved with salivary cancer
http://www.ncbi.nlm.nih.gov/pubmed/19559968

(i think the EBV uses the alpha estrogen receptors)

EBV and sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/1848394
http://www.ncbi.nlm.nih.gov/pubmed/1664987
http://www.ncbi.nlm.nih.gov/pubmed/1319486
http://www.ncbi.nlm.nih.gov/pubmed/3021847

HHV8 and sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/9003115

HHV8 binds the alpha estrogen receptor
http://d-scholarship.pitt.edu/13517/

retrovirus and sjogren's subgroup
http://www.ncbi.nlm.nih.gov/pubmed/9155673
http://www.ncbi.nlm.nih.gov/pubmed/8531355
http://www.ncbi.nlm.nih.gov/pubmed/1628425

Rank receptor and sjogren's
http://rheumatology.oxfordjournals.org/content/42/suppl_1/144.full.pdf

Rank receptor and HIV (thrombopoietin-like receptor and retrovirus)
http://www.ncbi.nlm.nih.gov/pubmed/22842843

Sjogren's syndrome is an autoimmune disease of the moisture producing glands

salivary secretion inhibited by activation of cannabinoid receptors
 I suspect HPV viruses for some cases
http://www.ncbi.nlm.nih.gov/pubmed/16946411

high rates of HPV with sjogren's patients?
http://www.blackwellpublishing.com/acrmeeting/abstract.asp?MeetingID=781&id=95227

no correlations found here??? hpv and sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/17713098

failure to find HPV in primary sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/10323467

which CB receptors are there?

both CB1 and CB2
http://www.physoc.org/proceedings/abstract/Proc%20Physiol%20Soc%2021PC38
http://www.ncbi.nlm.nih.gov/pubmed/16946411

mainly CB1?
http://www.scielo.cl/pdf/ijmorphol/v33n2/art44.pdf

If CB1 then HPV16?
http://angelabiggs.blogspot.com/2016/08/cannabinoid-receptors-and-human.html

HPV16 and EBV in salivary cancer
http://www.ncbi.nlm.nih.gov/pubmed/27547238

erosive oral lichen and hpv16
http://www.pasteur.fr/en/institut-pasteur/press/press-documents/human-papillomavirus-linked-auto-immune-disease

EOL and sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/2018610
http://www.ncbi.nlm.nih.gov/pubmed/2077152

spirochetes and lichen sclerosis
http://www.ncbi.nlm.nih.gov/pubmed/2393064
http://www.ncbi.nlm.nih.gov/pubmed/3192771
http://www.ncbi.nlm.nih.gov/pubmed/10792212
I can't tell if this is truly the lyme spirochete or not.

do spirochetes in humans move to the salivary gland like they do in ticks?

EOL, SJ and hepatitis C?
http://onlinelibrary.wiley.com/doi/10.1111/j.1346-8138.1997.tb02733.x/abstract?systemMessage=Wiley+Online+Library+will+be+unavailable+on+Saturday+3rd+September+2016+at+08.30+BST/+03:30+EDT/+15:30+SGT+for+5+hours+and+Sunday+4th+September+at+10:00+BST/+05:00+EST/+17:00+SGT+for+1+hour++for+essential+maintenance.+Apologies+for+the+inconvenience

http://onlinelibrary.wiley.com/doi/10.1111/j.1346-8138.1995.tb03395.x/full

Enteroviruses and nicotine acetylcholine receptors..does polio and d68 use the muscarine acetylcholine receptors or the ganglion nicotine receptors? can a nicotine patch help?

These are all ideas of how to slow the d68 infection but the AFM is probably caused by autoimmune cross-targeting where it is the body's own immune system that causes the paralysis.
http://angelabiggs.blogspot.com/2018/10/is-autoimmune-triggered-paralysis.html

It is the immune system we need to stop in order to stop the paralysis. There are ideas for kids with eczema/asthma who I feel are in the high risk group of developing the autoimmune disease due to the staph infection cross-targeting with d68. 

Rabies binds the neurotoxin binding site of the nicotinic acetylcholine receptor
http://www.ncbi.nlm.nih.gov/pubmed/8887475

This neurotoxin binding site is where nicotine binds
http://www.ncbi.nlm.nih.gov/pubmed/3448605

coxsackie virus (an enterovirus) infection is blocked by nicotine
http://www.ncbi.nlm.nih.gov/pubmed/26851533
http://www.ncbi.nlm.nih.gov/pubmed/26507386
http://www.ncbi.nlm.nih.gov/pubmed/26851533

Enteroviruses might bind the same receptor family as the rabies virus.

Hypothesis:
Enveloped virus families bind specific receptor families.

Looking at the types of nicotine binding receptors:
https://en.wikipedia.org/wiki/Nicotinic_acetylcholine_receptor

4 subtypes (these can be further divided)

Can we match up the enteroviruses with these receptors?

2 type the exists in the spine/ ganglion (GS) sympathetic and parasympathetic (GP)

2 types in the brain (B1 and B2)

one type exists in muscles (M)

Coxsackie appears to be using the Muscle type

non-polio enteroviruses are responsible for half of aseptic meningitis in children
http://www.ncbi.nlm.nih.gov/pubmed/17668054

Are most non- polio viruses using B1 and B2 but typically don't have access to the brain due to the blood brain barrier?

Do these viruses bind everywhere that nicotine does? Wouldn't it be strange if during enterovirus infections nicotine was given medically? or does polio and d68 bind muscarine ACH not nicotine ACH?

prozac and acetylcholine receptors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC20039/

prozac and d68 paralysis
http://www.neurologyadvisor.com/general-neurology/prozac-enterovirus-d68-paralysis-treatment/article/403896/

Prozac, that inhibits the replication of the virus, does not seem to reverse the d68's AFM
https://www.empr.com/news/fluoxetine-enterovirus-antiviral-acute-flaccid-myelitis/article/814285/

entroviruses could also bind "neural cell adhesion molecule"
http://jvi.asm.org/content/72/9/7181.full

D68 and sialic acid immunoglobulin like dependent entry
https://www.ncbi.nlm.nih.gov/pubmed/26563423
http://www.nature.com/ncomms/2015/151113/ncomms9865/full/ncomms9865.html

anti-nACH receptors with immunoglobulin antibodies (commercially made)
http://www.ncbi.nlm.nih.gov/pubmed/20619959 

rabies virus and sialic acid binding of receptors
http://www.ncbi.nlm.nih.gov/pubmed/8004936

rabies binding the muscarine ACH
https://www.ncbi.nlm.nih.gov/pubmed/15804965

Acetylcholine receptors and sialic acid
https://www.ncbi.nlm.nih.gov/pubmed/20487973

these overlaps supports the notion that the enteroviruses use ACH receptors but which one?

sialic acid dependent entry of D68
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4660200/

Enterovirus 71 infection blocked by:  heparin, polysulfated dextran sulfate, and suramin 
http://jvi.asm.org/content/87/1/611.full

estrogen and acetylcholine
file:///Users/angelabiggs/Downloads/Crosstalk_between_nicotine_and_estrogen-induced_estrogen_receptor_activation_induces_alpha9-nicotinic_acetylcholine_receptor_expression_in_human_breast_cancer_cell.pdf

silicone replacing silicon

Silicon is normally absorbed by the body.

silicon and bone health
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658806/

silicone or silicone: natural substance or artifical
http://www.livescience.com/37598-silicon-or-silicone-chips-implants.html

our body would not view silicone as natural

where silicon is found in the body:

hair and nails
blood vessels
skin
kidneys
lungs
bladder
adrenal cortex
prostate
testes

If silicone replaces the silicon slowly over time the body would react with inflammation, much like a viral infection.  The silicone is viewed as foreign.

Things however can become worse if an infection cross-targets with the silicone then autoimmune disease could be triggered.

Hypothesis: Enveloped virus families bind specific receptor families.

Hypothesis title:
Enveloped virus families bind specific receptor families.

Abstract:
Enveloped viruses are known to use receptors to trigger endocytosis into host cells.  Looking at the infection patterns of virus families, there exists a corresponding receptor family.  As the viral key mutates over time the receptor it uses slightly changes but only slightly.  The mutated new virus tends to stay within the receptor family.  If we understand the homology of receptors and their tissue expression patterns, the new virus' receptor choice should be to some degree predictable. The goal of this paper is to establish the virus families with their corresponding receptor families.

Introduction:
Vaccines prepare the immune system for viral infections. Current viral drugs attempt to inhibit viral replication.  This hypothesis supplies another avenue for defeating viral infections. If we know what receptors the viruses are using we can anticipate and slow the viral infection of host cells by competing for those receptors.

There are 4 major enveloped viral families we can immediately see this pattern with: flaviviruses, herpes viruses, flu viruses, and human papilloma viruses.  If you look at the infection patterns of these viral families it becomes clear that the herpes viruses use estrogen receptors, flaviviruses use melanocortin receptors, flu viruses use dopamine receptors, and human papilloma viruses use cannabinoid receptors.

Even more striking is that if you assume that a virus within it's virus family has an ideal receptor that it uses as an entry point into a host cell you can deduce which specific receptor this virus is using based on the symptoms of the illness caused by the virus.

The flavivirus family for example if it uses the melanocortin receptors appear to have this simple pattern:

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)
                     
mcr5  Dengue (immune system T cells)

The reactivation of herpes viruses seem to be affected by estrogen.  There are 3 types of herpes viruses which if you look at where they infect match up with the types of estrogen receptors.

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)

Flu viruses appear to use dopamine receptors:

Here is how the 5 types of dopamine receptors (D) that might match up with the A, B, and C flu viruses

D1 and D5 are similar but have reverse expression patterns.  D5 has the highest expression at birth then it decreases. D1 slowly increases in your life and is at it's lowest at birth.

D1 is the most abundant of the central nervous system. ( D1 and D5 )

D1 type B flu (encephalitis)

D5 type C flu (infects infants)

D2 is similar to D3 and D4.   D2 is expressed on the pancreas.

Type A flu and D2 receptors ( H1N1 and D3/D4 )

I am currently trying to elucidate other viral families. The receptor patterns have not been as obvious.

Enteroviruses (coxsackie, polio etc) may bind nicotine receptors
http://angelabiggs.blogspot.com/2016/08/enteroviruses-and-nicotine.html

The  Paramyxoviridae (measles family viruses) may bind the Muscarinic receptors 

http://angelabiggs.blogspot.com/2016/09/do-paramyxoviridae-measles-family.html

5 types of dopamine receptors and the A, B, and C flu viruses

Here is how the 5 types of dopamine receptors might match up with the A, B, and C flu viruses (hypothesis)

D1 and D5 are similar but have reverse expression patterns.  D5 has the highest expression at birth then it decreases. D1 slowly increases in your life and is at it's lowest at birth. 

D2 is similar to D3 and D4

D1 is the most abundant of the central nervous system. ( D1 and D5 )

D2 receptors are expressed on the pancreas

http://www.jbc.org/content/280/44/36824.long

Type A flu viruses appear to infect pancreatic cells

http://jvi.asm.org/content/87/1/597.full

H1N1 and narcolepsy 

http://www.ncbi.nlm.nih.gov/pubmed/25320099

D2 receptors and narcolepsy connection in dogs

http://www.ncbi.nlm.nih.gov/pubmed/3828787

D3 and D4 receptors are expressed in the human heart

http://www.ncbi.nlm.nih.gov/pubmed/12117307

H1N1 infects the heart

http://www.sandiegouniontribune.com/news/2010/feb/23/h1n1-flu-can-attack-heart/

Type A 8 RNA segments  and D2 receptors?  H1N1 and D3/D4 ?

bird flu H5N1

asian flu H2N2

hong kong flu H3N2

swine H1N1 russian flu / spanish flu 

Type B (?)  8 RNA segments and D1 receptors? (no diabetes triggered)

encephalitis linked to flu type B

http://cid.oxfordjournals.org/content/36/7/e87.full.pdf

H3N2
http://www.cidrap.umn.edu/news-perspective/2014/05/cdc-dont-take-influenza-b-lightly-adults

Type C  (humans and pigs only) 7 RNA segments  and D5 receptors? 

causes pediatric pneumonia 

http://www.upmc-cbn.org/report_archive/2013/cbnreport_01112013.html

Vaccines contain two type A and one or two type B flu viruses.

Attempting to match up herpes viruses with estrogen receptors

Are the herpes viruses binding different estrogen receptors?

The locations of the receptors seem to match up with the herpes virus families. (these are not proven associations)

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 alpha receptors on lymphocytes
http://www.ncbi.nlm.nih.gov/pubmed/18569528

Review paper that covered the distinct variations of alpha estrogen receptors (different isoforms)
http://physrev.physiology.org/content/87/3/905

Looking at isoforms could further divide up the virus families even more specifically.

papers referenced with isoforms discoveries

http://emboj.embopress.org/content/19/17/4688?ijkey=05415c28b4fcc9840305690efd14a4351fec1884&keytype2=tf_ipsecsha

http://www.ncbi.nlm.nih.gov/pubmed/16165085?access_num=16165085&link_type=MED&dopt=Abstract

ERalpha 66 and breast cancer and ERalpha 36 is the truncated form
http://www.ncbi.nlm.nih.gov/pubmed/18383888

ERRalpha and CMV (HHV4)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284536/

EER is the "estrogen related receptor " which has homology to the estrogen receptor alpha but does not bind estrogen rather estrogen like ligands
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284536/

HHV8 EREs were found to bind alpha estrogen receptors
http://d-scholarship.pitt.edu/13517/

Estrogen alpha receptor and breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/14973389

Extremely high IFN with alphaviruses and flaviviruses? is it more than the typical increase because of NS1?

IFN was once called viral inhibitory factor.  

IFNs are the cytokines released by host cells to call the immune system to come fight an infection. IFN is responsible for the "flu like symptoms" of high fever and muscle pains.

However when alphaviruses and flaviviruses are involved it almost seems as if IFN overdosing is occurring. why is IFN so high?

These viruses secrete NS1.

NS1 a protein that these viruses secrete which alters IFN expression
http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0013927

Immediately proceeding infection by alphaviruses " alphavirus-infected cells become unable to respond to IFN-β"
http://www.ncbi.nlm.nih.gov/pubmed/22345447

sindbis virus and IFN receptor mutant mice...died of hemorrhagic fever
http://www.sciencedirect.com/science/article/pii/S0042682207004175

completely blocking IFN stops the hemorrhagic fever
https://www.scripps.edu/newsandviews/e_20140616/baccala.html

IFN was found to be critical for Venezuelan equine encephalitis virus 
http://www.ncbi.nlm.nih.gov/pubmed/11264360

Further when a group attached a green fluorescent protein to Ross River Virus they could see that initially the virus acts through macrophages
http://www.labonline.com.au/content/life-scientist/news/ross-river-study-offers-arthritis-clues-833562532

MCr 1 and MCR3 are on macrophages (see below links to why i think these viruses infect using these receptors)
http://www.ncbi.nlm.nih.gov/pubmed/22566831

IFN gamma is the key macrophage activator
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630590/

there are 2 pathways a macrophage could go: one increases the inflammatory response and the other decreases the inflammatory response
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4316183/figure/fig01/

binding IFN makes macrophages into type one which does not secrete il-10
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4316183/

il-10 has a strong connection to arthritis where it regulates inflammasome. il-10 is an anti-inflammatory cytokine.
http://arthritis-research.biomedcentral.com/articles/10.1186/s13075-014-0419-y

Inflammasome is a multiprotein complex that triggers inflammation

Alphaviruses/flaviviruses cause severe joint pain and inflammation (through the lack of il-10 when the wave of IFN occurs when the immune system overcomes ns1?)

ns1 increases il-10 (in the flaviviruse dengue initially in infection)
http://www.ncbi.nlm.nih.gov/pubmed/26621477

So in the initial stage, flaviviruses and alphaviruses through ns1 suppresses ifn and increases il-10 in an attempt to block normal viral inflammation.  However somehow the immune system overcomes this ns1 protein and makes massive amounts of IFN.

 IFN has been found in the of RA patients synovial fluid (not connected to this disease but the feature of joint pain with the presence of IFN could be significant)
http://www.ncbi.nlm.nih.gov/pubmed/20166872

alphaviruses can have swollen lymph glands

IFN and lymph node development
http://www.pnas.org/content/100/23/13453.full.pdf

IFN pathways and lipopolysaccharide disrupted by River Ross virus
suppressed
http://www.ncbi.nlm.nih.gov/pubmed/12364588

are there known connections between IFN and alphaviruses : Their replication is sensitive to IFN?
http://www.ncbi.nlm.nih.gov/pubmed/25927359

IFN gamma has an affect on skin and pigment so it has some receptors
http://www.ncbi.nlm.nih.gov/pubmed/14760888

IFN beta medication causing skin rash: erythematous maculopapular rash 
http://www.ncbi.nlm.nih.gov/pubmed/18337427

This maculopapular rash is also called morbilliform, it looks like the measles, and is found in all alphavirus cases.

chikungunya and maculopapular rash
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856378/

O'nyong-nyong and maculopapular rash
http://wwwnc.cdc.gov/eid/article/20/10/14-0823_article

IFN alpha and chorea
http://www.ncbi.nlm.nih.gov/pubmed/11805273

types of alphaviruses:

chikungunya
ross river
mayaro
Barmah forest
sindbis
o'nyong nyong

alpha virus family tree link
http://www.sciencedirect.com/topics/page/Mayaro_virus

chikungunya
https://www.jci.org/articles/view/40104

high IFN and asthma
https://www.jci.org/articles/view/80911
https://aacijournal.biomedcentral.com/articles/10.1186/1710-1492-8-18
(non-atopic asthma in latin american children?...not related to allergy)

chikungunya and asthma
http://www.ncbi.nlm.nih.gov/pubmed/20513912

the liver has IFN-beta receptors (medical dosing of IFN beta has resulted in liver damage)
http://www.ncbi.nlm.nih.gov/pubmed/16531969

rhabdomyolysis and alphaviruses??? is it caused by the high IFN levels???
http://www.ncbi.nlm.nih.gov/pubmed/20962735 chikunguya
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000527 chikunguya (muscle satellite cells?)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242063/ ross river

rhabdomyolysis after IFNbeta treatment (a known condition from high levels of IFN)
http://www.ncbi.nlm.nih.gov/pubmed/27456881
http://www.ncbi.nlm.nih.gov/pubmed/25008446
http://jnnp.bmj.com/content/72/2/274.1.full
http://www.nature.com/ajg/journal/v98/n4/full/ajg2003222a.html
http://jco.ascopubs.org/content/19/17/3794.full
http://jac.oxfordjournals.org/content/67/1/249.long
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(97)80091-8/abstract
http://www.msard-journal.com/article/S2211-0348(16)30057-8/abstract

Alphaviruses like flaviviruses use melanocortin receptors to infect.

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

my previous ideas of flaviviruses and melanocortin receptors
http://angelabiggs.blogspot.com/2016/08/do-all-flaviviruses-to-some-degree-bind.html

Do all flaviviruses to some degree bind MCR1? (in addition to their main melanocortin 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)
                       
mcr5  Dengue (immune system T cells)

I am thinking they open the door into cells using this receptor most of the time and the other melacortin receptors less well.

Fantastic MCR review paper
http://pharmrev.aspetjournals.org/content/56/1/1.full

However do all the flaviviruses bind mcr1 weakly?

Mcr1 is at the skin and could be the reason for the flavivirus skin rashes/melanoma link

mcr1 and skin
http://www.ncbi.nlm.nih.gov/pubmed/10597134

mcr1 and melanoma
http://www.ncbi.nlm.nih.gov/pubmed/24460937

mcr1 translocates to the nucleus? hmmm or just being made
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4885833/
https://www.ncbi.nlm.nih.gov/pubmed/9362391

Red hair has the mutation to mcr1 and it has been long known that they have much higher rates of melanoma which could mean the virus binds these receptors better?

Red heads typically require more anesthetics

mcr1 mutations and pain
http://www.ncbi.nlm.nih.gov/pubmed/15994880

What about the joint pain that all flaviviruses can develop?

Joints:

Could the MCR1  help explain the delayed joint pain experienced in dengue?
http://timesofindia.indiatimes.com/city/pune/Post-dengue-joint-and-muscle-pain-on-rise/articleshow/44936280.cms

Mcr1 has been looked at concerning joints and osteoarthritis. (so the receptors are there in the joints the question is does the virus infect using them causing the dengue's pain in later stages)

http://www.ncbi.nlm.nih.gov/pubmed/25191747

Blindness and blood shot eyes:

the blood shot eyes that are associated with the flaviviruses are caused by inflammation of the ocular
http://emedicine.medscape.com/article/1192122-overview

mrc1 is expressed at the ocular (studies in red heads)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1180688/

Could the blindness occur when the virus has destroyed too many ocular cells? Does eye sight weaken after flavivirus infections in general?

dengue and blindness
https://www.evrs.eu/severe-blindness-a-rare-but-devastating-complication-of-dengue-fever/

westnile and blindness (mcr 3 or mcr 1)
http://www.ncbi.nlm.nih.gov/pubmed/16344453
http://www.ncbi.nlm.nih.gov/pubmed/15621074
http://forums.studentdoctor.net/threads/effects-of-west-nile-virus-on-vision.259316/

Zika and blindness (mcr4 or mcr 1)

http://www.usnews.com/news/articles/2016-05-25/study-suggests-zika-causes-blindness

ocular melanoma and mcr1

http://www.ncbi.nlm.nih.gov/pubmed/17325166

Prostate cancer seems to be linked to all the flaviviruses too

could this be because the prostate has mcr1?

MCR2 and prostate cancer
https://www.ncbi.nlm.nih.gov/pubmed/22842514

(assuming my co-carcinogenesis hypothesis that a carcinogen and a virus together cause most cancers thus explaining the link between melanoma and prostate cancer)

link for mcr4 and liver
https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0030-1269482

Mcr4 mutations have been linked to obesity

it is then interesting to see that vaccines for yellow fever which might use mcr4 have had a metabolic response
http://www.ncbi.nlm.nih.gov/pubmed/7010983

hepatitis C and encephalitis
http://www.ncbi.nlm.nih.gov/pubmed/15554429
http://www.ncbi.nlm.nih.gov/pubmed/12614463
http://www.ncbi.nlm.nih.gov/pubmed/16251811

hepatitis and thrombocytopenia (mcr1)
http://www.ncbi.nlm.nih.gov/pubmed/21188328

Note that Hep C infections was not found to increase melanoma risk.  So is it west nile and the MCR3 receptor?