Wednesday, May 17, 2017

Hypothesis: virus families use receptor families (with references)


Angela Biggs
May 17, 2017

Hypothesis: Virus families use receptor families.

Abstract:  Based on the information available 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 3 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.  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, 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.  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.

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, enteroviruses with acetylcholine receptors,  reoviruses with  beta-adrenergic receptors, human papillomaviruses with cannabinoid 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, ChacĂ­n-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.


Tuesday, May 16, 2017

Contemplations of Synuclein, glutamate secretion, and Autoimmune Parkinson's disease

Considering Autoimmune cross-targeting as the trigger of Parkinson's, two infections on one target where a virus is inside and a larger infection is outside.  Why do we see the characteristics we see for parkinson's disease?

Hypothesis:  The pathways of the receptor used by the virus causes the distinctive features of the autoimmune disease.

Altered glutamate transmission is the core of parkinson's
https://www.google.com/search?q=glutamate+parkinson%27s&oq=glutamate+parki&aqs=chrome.0.0j69i57j0l4.5606j0j4&sourceid=chrome&ie=UTF-8

synuclein plaques are the hallmark of Parkinson's

How does synuclein connect to glutamate?

alcohol and cocaine increase synuclein in brain

both cause increases in glutamate release

 stimulation of the nerves by glutamate sends PARKIN to the mitochondria

PARKIN was discovered as the genetic mutation found in familia, genetic, parkinson's disease

HIGH glutamate or further down the path...over sensitive Parkin 

Parkin causes the autophagy of mitochondrias (their destruction)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2592826/

less functional nerves makes it look a lot like the death of nerves...which is the case for autoimmune parkinson's disease

So does synucleins represent nerves stuck in secretion mode? 

What causes this state of synucleins to precipitate and the neuron to be stuck secreting? A virus would typically have destroyed the cell making new viruses. 

Parkinson's is an autoimmune disease where antibodies against synucleins have developed.

 Autoimmune disease cross-targeting occurs when 2 infections exist on one target, one inside and one outside and self protection has broken down. (if you are attacking the outside and the inside there is no protection occurring)

All nerve cells with synuclein attacked? 

dermal skin nerve synucleins in those with REM sleep disorder Parkinsons
https://www.ncbi.nlm.nih.gov/pubmed/28180961

dermal skin nerve synucleins in those with Multiple system atrophy
https://www.ncbi.nlm.nih.gov/pubmed/26175301

even the gut of parkinson's patients has synuclein clumps!
http://www.livescience.com/36354-parkinsons-disease-colonoscopy-diagnosis.html

mycobacteria in parkinson's and crohn's
https://www.ncbi.nlm.nih.gov/pubmed/?term=crohn%27s++synuclein

Guts of crohn's did not have synuclein until parkinson's developed
http://www.livescience.com/36354-parkinsons-disease-colonoscopy-diagnosis.html

which indicates this is not mycobacteria specific but rather when perhaps a virus shows up too.

However, neither alzheimers or chicken pox increase synuclein which might explain parkinsonism.  The killing of nerves and not a specific focus on synuclein type.

Review with a focus on why these specific viruses: flu and flaviviruses

Synuclein is required for glutamate release (as linked before)
https://www.ncbi.nlm.nih.gov/pubmed/17689254

If syn which is involved with the vesicles and secretions of Glutamate by neurons is precipitating in parkinson's disease thus forming the signature synuclein plaques because the demand for glutamate  has increased? more transport vesicles moving the glutamate....extra synuclein proteins...neurons  stuck in secretion mode.

Is Parkinson's a state of over secretion of glutamate?

The amount of glutamate does appear to be increased in Parkinson's disease patients.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030918

cAMP dependent Glutamate release
http://www.jbc.org/content/271/48/30554.full.pdf

D2 (dopamine receptor) activation inhibits cyclase activity (which converts ATP to cAMP)

D2 is used by the flu virus to enter the cell which would raise glutamate (stimulating the receptor as the virus entered)

avian flu increases synuclein

flu viruses appear to use dopamine receptors

synuclein alters number of dopamine receptors

synuclein also appears with west nile virus infections

note that neuromelanin is now thought to cause synuclein

does secretion of melanin require synuclein? 

neuromelanin accumulation and increased synuclein

west nile uses melanocortin receptor 3 (west nile infects the kidney too)

Parkinson's has been connect to two cancers: non hodgkin lymphoma and melanoma

Hepatitis C another flavivirus has also been linked to parkinson's

non hodgkin lymphoma and hep C




















Wednesday, May 10, 2017

Virus families use receptor families: Paper attempt

Hypothesis: Virus families use receptor families.

Abstract:  Based on the information available there is substantia  l 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 they entered cells using different receptors like doorknobs.  Subsequent research matching viruses to receptors reveals the possibility that virus families use receptor families.  The following paper will be a review of 3 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, SV40, 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 and SV40 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.  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, 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.  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.


Polyomaviruses and serotonin receptors

Bk virus and ganglioside receptors
https://www.ncbi.nlm.nih.gov/pubmed/16415013

SV40 and ganglioside receptors
https://www.ncbi.nlm.nih.gov/pubmed/12941687

JC virus and serotonin receptors
https://www.ncbi.nlm.nih.gov/pubmed/15550673

SV40 transgenic mice over express serotonin receptors
https://www.ncbi.nlm.nih.gov/pubmed/3022874

serotonin receptors were once considered a type of ganglioside receptor

Herpes viruses and Estrogen receptors

herpes HHV1 reactivation is estrogen receptor dependent 2010
https://www.ncbi.nlm.nih.gov/pubmed/19846508

HHV1 or HHV2 infections stimulated Estrogen receptor production (by using the existing ones?)
https://www.ncbi.nlm.nih.gov/pubmed/2539527

HHV8 and the estrogen receptor alpha 2008 (unpublished?)
http://d-scholarship.pitt.edu/8097/

Estradiol and CMV
https://www.ncbi.nlm.nih.gov/pubmed/3011615

Estradiol increases the number of progesterone and estrogen receptors
https://www.ncbi.nlm.nih.gov/pubmed/9160720

Flaviviruses and melanocortin viruses

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

Hep C seems to have diseases that overlap Griscelli syndrome
http://angelabiggs.blogspot.com/2017/05/flaviviruses-melanocortin-receptors-and.html

Griscelli syndrome is the appearance of silver gray hair starting in infancy and hypo-pigmentation diagnosed as partial albinism.  Griscelli syndrome appears to be a genetic disorder where there is disrupted transport of melanosomes, melanin pigment containing vesicles.  What is fascinating about this is that Griscelli syndrome is also associated with neutropenia, thrombocytopenia, and NK cell dysfunction.

Primed T cells express mcr5
http://www.ncbi.nlm.nih.gov/pubmed/11488983

More receptors and viruses with further detail
http://angelabiggs.blogspot.com/2017/04/hypothesis-virus-families-find-receptor.html

found virus history review
https://rybicki.wordpress.com/2012/02/06/a-short-history-of-the-discovery-of-viruses-part-1/

1982 Rabies and acetylcholine
https://www.ncbi.nlm.nih.gov/pubmed/7053569

Flaviviruses, Melanocortin receptors, and NK cells: Hepatitis C


Hepatitis C and NK cell dysfunction
https://www.hindawi.com/journals/bmri/2014/903764/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817297/
https://www.ncbi.nlm.nih.gov/pubmed/16234066

When you consider the autosomal recessive disorder Griscelli syndrome and interesting overlap appears.

Griscelli syndrome is the appearance of silver gray hair starting in infancy and hypo-pigmentation diagnosed as partial albinism.  Griscelli syndrome appears to be a genetic disorder where there is disrupted transport of melanosomes, melanin pigment containing vesicles.  What is fascinating about this is that Griscelli syndrome is also associated with neutropenia, thrombocytopenia, and NK cell dysfunction.

Hepatitis C has been connected to thrombocytopenia
https://jmedicalcasereports.biomedcentral.com/articles/10.1186/1752-1947-8-303
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5333732/
https://www.ncbi.nlm.nih.gov/pubmed/21188328
https://www.ncbi.nlm.nih.gov/pubmed/19154665

Hepatitis C has been connected to neutropenia
http://journals.lww.com/co-hematology/Abstract/2014/01000/Hepatitis_C_and_neutropenia.11.aspx
https://academic.oup.com/cid/article/doi/10.1086/376971/331606/Hematologic-Disorders-Associated-with-Hepatitis-C
http://hepatitis.cl/wp-content/uploads/2012/08/2002-1-Neutropenia-associated-with-alpha-interferon-therapy-of-chronic-hepatitis-C.pdf

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)


NK cells and Tickborne encephalitis virus
http://www.jimmunol.org/content/early/2016/08/19/jimmunol.1600950.short

MCR1 and melanosome
http://www.jimmunol.org/content/early/2016/08/19/jimmunol.1600950.short







Monday, May 8, 2017

MCR4, Hep C, glucose metabolism, and HCC (heptocellular carcinoma): pattern reveals a distinctive Type2 diabetes

liver cells stop making glucose as they become cancerous
https://www.sciencedaily.com/releases/2012/07/120730141635.htm

MCR4 and glucose metabolism...so so through insulin?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033043/

Hepatitis C, insulin resistance, and HCC
https://www.ncbi.nlm.nih.gov/pubmed/20458764

Hepatitis C and insulin resistance
https://www.sciencedaily.com/releases/2010/03/100309102519.htm

melanocortin hormone and insulin resistance
https://link.springer.com/article/10.2165/00024677-200605010-00002

the glucose transporter suppresses the melanocortin receptor
http://www.endocrine-abstracts.org/ea/0041/ea0041EP809.htm

melanocortin increases GLUT expression? and alters glucose metabolism?

melanocortin antagonist increases insulin sensitivity
http://www.sciencedirect.com/science/article/pii/S0196978104002050
http://www.sciencedirect.com/science/article/pii/S0014579307001652

over expression of agouti caused increased growth not obesity
https://www.ncbi.nlm.nih.gov/pubmed/27156808

HCC and GLUT-2 (glucose transporter)
https://www.ncbi.nlm.nih.gov/pubmed/18949368

HCC and GLUT-1
https://www.ncbi.nlm.nih.gov/pubmed/19874261
https://www.ncbi.nlm.nih.gov/pubmed/19286567

(so there must be two types of type 2 diabetes: hepatitis C type and the mycobacteria type)

hep C and type 2 diabetes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669937/

The mycobacteria type overlaps psoriasis, chron's, parkinson's and has fatty liver disease with high cholesterol.  The issue with mycobacteria is that the quorum is cGMP which messes with our cells glucose transporter.

In the case of hep C the triggering of the melanocortin 4 receptor pulls the glucose transporters from the membrane and changes the glucose metabolism through gene changes. We should be able to sort these 2 types of diabetes out from each other.

Hep C causes the liver to scar (cirrhosis) over time.  The liver cells are not just dysfunctional they are dying.

Damage to other organs infected by hep C  has started to emerge.

Pulmonary fibrosis (scarring lung damage)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3206667/

Scarring of the colon could be what causes diverticulitis, the scars cause the colon to fold, explaining the "left colon cancer" connection
https://www.ncbi.nlm.nih.gov/pubmed/8555344

The non-Hodgkin's lymphoma called nodular sclerosis, which is the most common kind, is filled with fibrous scars.
https://en.wikipedia.org/wiki/Nodular_sclerosis

hep c and non-Hodgkin's lymphoma
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802504/

overlap of B cell and nodular lymphoma
https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-14-332

Liver, colon, and lung cancers have been linked to hep C....along with a huge list of other cancers.

other overlapping disorders linked to hep C can help us separate the diabetes:

http://emedicine.medscape.com/article/1134161-clinical?pa=bNC91gt1rcVQirt7Fvkd%2FYuDdd7pFGHrK2nx0uRZFmz1FjlQja9m4jLs8Nzam%2B%2BuMvFliwSOoozYUdBPs1l8Qd1zi39gDfdraEJUUFno0Ig%3D

Lichen planus is the skin manifestation of hep C

And because Hep C also uses MCR1 Thrombocytopenia (red blood cells) can appear

The point is that the type 2 diabetes associated with Hep C will have completely different issues from the mycobacteria form.













Sunday, May 7, 2017

Cannabinoid 2 receptors, prostate cancer, breast cancer, HPV18, and olive oil????

I am currently collecting papers of overlap but a pattern seems to be emerging with Cannabinoid 2 receptors in the center.

HPV16 for squamous and HPV18 for adenocarcinoma (basal cell)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361088/

cannabinoid 2 receptor regulation of prostate cancer
http://grantome.com/grant/NIH/U54-CA156735-02-5707

olive oil and CB2 receptor
http://content.iospress.com/articles/nutrition-and-healthy-aging/nha160008

Olive oil, prostate cancer and survival
http://www.npr.org/sections/thesalt/2013/06/10/190360777/hey-fellas-olive-oil-and-nuts-tied-to-prostate-cancer-survival

Olive oil and breast cancer risk
http://www.health.harvard.edu/womens-health/research-were-watching-high-olive-oil-consumption-linked-to-lower-breast-cancer-risk

cannabis THC binds the CB1 receptor (the nerve slowing reaction)  and the CB2 receptor which might be the reason for the munchies?

CB2 receptors are increased in breast cancer
https://www.ncbi.nlm.nih.gov/pubmed/27213582

but Squamous breast cancer is rare
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3931217/

most triple negative breast cancer is basal like...are most hpv18?

HPV and breast cancer ?
https://infectagentscancer.biomedcentral.com/articles/10.1186/s13027-016-0058-9
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0172760

HPV and actinic keratosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3642014/

Basal cell carcinoma and actinic keratosis have increased phospholipids
https://www.ncbi.nlm.nih.gov/pubmed/10397583

CB1 receptor and CB2 receptor antagonists increase lipids in liver (fatty liver )
https://www.ncbi.nlm.nih.gov/pubmed/20602678

Clear cell carcinoma has lipid metabolism issues causing the yellow look of the cells

Clear cell

Clear cell renal cell carcinoma and HPV

HPV and renal cell carcinoma
http://onlinelibrary.wiley.com/doi/10.1002/jmv.23945/abstract

clear cell penis carcinoma is squamous HPV
http://journals.lww.com/ajsp/Citation/2016/07000/Clear_Cell_Carcinoma_of_the_Penis___An_HPV_related.6.aspx

HPV does demethylation

Clear cell renal cell carcinoma and herv E
https://www.ncbi.nlm.nih.gov/pubmed/26862115

Clear cell cancer and cannabinoid receptors of the CB1 type are decreased? and CB2 is not expressed?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989249/

Here they found over expression of CB1: but they are not specific which kind of RCC
https://www.springermedizin.de/overexpression-of-cannabinoid-receptor-1-promotes-renal-cell-car/10898958

( HPV16 seems to use CB1)

clear cell renal carcinoma actually have a golden yellow appears due to an accumulation of lipids
http://emedicine.medscape.com/article/1612043-overview?pa=58O8ipQc5%2Buu2M08DeBeRLaqlzPm8CfcZzRXra9ztt%2BlokvVNZ%2FAwbhQ5uyMd8txHhCnHvXnShVL70%2Fs9Tn3YrOwhd8Mdk7tVO%2FdkscsGC4%3D

clear cell renal carcinoma seem to lipid issues connect to ceramide levels
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0172632

CB1 cannabinoid receptor one is connected to ceramide
https://www.ncbi.nlm.nih.gov/pubmed/15958274

note that clear cell carcinoma of the cervix is hpv18 which uses the CB2 receptors
http://journals.lww.com/intjgynpathology/Abstract/2012/05000/Clear_Cell_Adenosquamous_Carcinoma_of_the_Cervix__.15.aspx

Papillary thyroid cancer into clear cell renal cancer
https://www.ncbi.nlm.nih.gov/pubmed/28249616

HPV16 and thyroid cancer
https://www.ncbi.nlm.nih.gov/pubmed/18985036

Clear cell of the head and neck connected to metastatic renal cell
http://www.sciencedirect.com/science/article/pii/S1741940904000172

Head and neck cancer with HPV16
https://www.ncbi.nlm.nih.gov/pubmed/24474236






Wednesday, May 3, 2017

Zika, ACTH receptors,adrenergic receptors, and tendon tightness

Noticed the green tape for muscle tightness in the article
https://www.nytimes.com/2017/05/01/health/zika-twins-transmission-theories.html?_r=0

Could Zika using ACTH receptors cause issues with tendons?

adrenergic control of cortisol and ACTH
https://www.ncbi.nlm.nih.gov/pubmed/1359600

high ACTH and adrenergic receptors
https://www.ncbi.nlm.nih.gov/pubmed/1968233

the alpha-adrenergic receptors is involved with the tendons of the finger

Dupuytene's contracture involves the tendons of the hand especially the ring finger and alpha-adrenergic receptors

What is going on with these Zika kiddos that gives them something like dupuytene's contacture?

Zika and joint problems with babies
https://www.usatoday.com/story/news/2016/08/08/study-links-zika-virus-joint-problems-babies/88416832/

zika babies also had brain calcifications....this really over laps with the reovirus group that has adrenergic receptor issues

when zika displaced the ACTH using the ACTH receptors then the level of ACTH interacting with other stuff occurred thus decreasing the amount of adrenergic receptors?

older posts of mine with Zika and the ACTH receptor
http://angelabiggs.blogspot.com/2016/05/the-zika-file.html
http://angelabiggs.blogspot.com/2016/03/acth-and-placenta.html
http://angelabiggs.blogspot.com/2017/01/zika-acth-receptors-and-clatherin.html