Gastric adenocarcinomas and co-carcinogenesis

Gastric (stomach) cancer

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 nobel prize)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen with a benzene ring inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications. Co-carcinogenesis requires a virus and a carcinogen to start the cancer. The cancer tumor wears the entry receptor on the surface.

The types of gastric cancer are:
Adenocarcinomas,  lymphomas, gastrointestinal stromal tumors, carcinoid tumors

This post will focus on Adenocarcinomas

Epstein-barr and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/25633561
http://www.ncbi.nlm.nih.gov/pubmed/26337667
http://www.ncbi.nlm.nih.gov/pubmed/11091849

estrogen receptors and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/2845639
http://www.ncbi.nlm.nih.gov/pubmed/7898114

Herpes viruses might be using the estrogen receptors. (which does explain how they end up in the mitochondria of nerves since the estrogen receptor cycles there, update...virus families use receptor families.  There are 3 types of herpes viruses and 3 types of estrogen receptors: alpha beta and estrogen-like.  Epstein barr would end up in the nucleus using the alpha estrogen receptor while zoster the mitochondria using the beta estrogen receptor)

Carcinogens of the digestive track?

H.pylori and sulfur
http://www.ncbi.nlm.nih.gov/pubmed/16721224

Sulfur as a carcinogen
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566939/

H.pylori increases the rate of stomach cancer
http://scienceblog.cancerresearchuk.org/2014/03/07/a-bugs-life-h-pylori-and-stomach-cancer/

H.pylori lowers the pH of the stomach (more acidic)

viruses infect better in lower pH
http://www.meridianinstitute.com/newslet/Vol7-3/7-3.html

Adenoviruses infect the stomach the most probably trigger the common stomach tumors

10% Gastric cancer and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528272/

epstein-barr and pernicious anemia
http://www.jle.com/en/revues/hma/e-docs/maladie_de_biermer_revelee_par_une_hepatite_a_epstein_barr_virus_271904/article.phtml

pernicious anemia and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/506804
http://www.ncbi.nlm.nih.gov/pubmed/3383791

estrogen receptors and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/2845639
http://www.ncbi.nlm.nih.gov/pubmed/7898114

Herpes viruses might be using the estrogen receptors. (which does explain how they end up in the mitochondria of nerves since the estrogen receptor cycles there)

Gastric carcinoid tumour associated with enteroviruses
http://www.ncbi.nlm.nih.gov/pubmed/21278394

Gastrointestinal stroma tumors and somatostatin receptors (hepatitis?)
http://www.ncbi.nlm.nih.gov/pubmed/23116418

Hepatitis B and gastric cancer????
http://www.ncbi.nlm.nih.gov/pubmed/26010504

Which viruses and receptors match up? Here are suspected matches:

These matches need to be verified. This are suspected not proven.


Melanocortin receptors and Flaviviruses (west nile, dengue, zika)

Estrogen receptors and Herpes viruses

Dopamine receptors and Flu viruses

Acetlycholine receptors and Enteroviruses (d68, coxsackie)

Cannabinoid receptors and Human Papilloma viruses

serotonin receptors and Polyomaviruses (JC virus/sv40, BK, hepatitis B)

luteinizing hormone receptors and retroviruses (rous sarcoma virus, HIV)

Muscarinic receptors and Paramyxoviridae (measles, mumps, RSV, parainfluenza viruses)

IFN receptors? and alphaviruses

Togaviruses are divided into two genera: Rubivirus and Alphavirus? what receptor does Rubella virus use?

NOTES:

Hepatitis A is an enterovirus
Hepatitis B is a polyomavirus
Hepatitis C is a flavivirus

note that gangliosides were the first receptor found  for serotonin

EGF-R and cannabinoid overlap

HPV infected cells increases EGF-R receptors
http://jnci.oxfordjournals.org/content/89/17/1271.full

there is a close relationship between EGF and cannabinoid
an inverse agonist of cannabinoid receptors have been show to increase EGF

nectin4 and Hemagglutinin receptors overlap
http://www.nature.com/nsmb/journal/v20/n1/full/nsmb.2432.html

somatomedin A is also IGF2

LH receptors might bind gangliosides and therefore the retroviruses (pituitary carcinomas) and Thrombopoietin?


membrane cofactor protein and Adenovirus: the common cold

Adenoviruses belong to the family Adenoviridae, and are divided into two genera, Mastasdenovirus (mammalian adenoviruses), and Aviadenovirus (avian or bird adenoviruses).

"We are what we eat” Do our cancer cells wear in high numbers the receptors the viruses used to infect them? Does Co-carcinogenesis explain most cancers?

Title:  “We are what we eat” Do our cancer cells wear in high numbers the receptors the viruses used to infect them?  Does Co-carcinogenesis explain most cancers?

Abstract:   Cancer cells appear to express the receptors that reveal the virus that triggered their cancerous tumor growth.  This hypothesis supports Co-carcinogenesis as the cause of cancer.
This paper will go through several types of cancer looking at the patterns of receptors on tumors, of the cancers that tend to appear together, and looking for the viruses that have been isolated from tumors.

Introduction:

 Francis Peyton Rous challenged the oncology world first when he suggested that cancers did not spontaneously occur but could be triggered by something in a contagious way.  Unbeknownst to him he was working with the Rous Sarcoma virus. (when the virus was discovered it was named after him)  He could see that he was transferring some agent from one chicken to another and triggering the tumors.  The oncology world seemed to believe that this was strictly a chicken pattern.  Unsuccessfully he alone attempted to isolate viruses from mammalian tumors for years.

 20 years later fellow researcher Richard Shope isolated HPV from mouse tumors. They now had a mammalian virus.  Fervently Rous and his coworker Friedewald studied the HPV virus attempting to prove that it triggered the tumors in mammals.  Their work on HPV got them the Nobel prize in 1966. 

One hypothesis of his, Co-carcinogenesis suggests that it is the synergistic actions of a virus and a carcinogen together on a host cell that causes cancer.  Both must be present. However the evidence of viruses can rarely be found in cancer cells. In petridishes viruses and carcinogens have been shown to produce cancer cells.  Perhaps because they are merely the triggers at the beginning.  Thus the oncology world has decided that only 20% of cancers are involved with viruses . 

Based on what we know of tumors, viruses, and receptors this paper will attempt to show that Rous and Friedewald’s Co-carcinogenesis could explain most of the cancers we deal with today. (1-3)

Hypothesis:  Cancer cells express receptors that reveal the virus that triggered their cancerous tumor process.  This hypothesis supports Co-carcinogenesis as the cause of cancer. 

Evaluation of Hypothesis:

Viruses are now known to make proteins that interact with the telemores which are the ends of our chromosomes. The condition of the telomeres, how frayed or pristine, determines how many times the chromosomes can be copied.  Viruses are therefor making our DNA, the cookbooks of our cells, immortal and open for use.  Carcinogens, such as benzene and phenols, are now known to have multiple actions including inhibiting polymerase which are the DNA readers.  Viruses typically make their own polymerases which have a stronger affinity for binding in order to compete with the host's polymerase. Now imagine them coexisting as Co-carcinogenesis suggests.  The DNA has been opened up but the viral polymerases are inhibited and a cancer cell has been created.  Is this possible? The virus when it enters a cell uses a specific receptor thus stimulates the production of more of those specific receptors to be made.  It is my contention that when we look at the cancerous tumors they will be overexpressing the receptor which tells us which virus triggered them. So let's look at a few cancers and see.

Breast cancer has 2 types. An estrogen receptor and non estrogen receptor type.  Interestingly enough 2 viruses have been isolated from breast cancer; the HPV virus and the Epstein-barr virus.  The Epstein Barr virus is likely using estrogen receptors.  In adrenal cells estrogen receptors cycle to the nucleus which would allow herpes viruses to interact with the nucleus but in nerves the estrogen receptors cycle to the mitochondria.  Herpes viruses are known to hide in the mitochondria of nerves and to travel down the nerves riding in the mitochondrias like little cars.  If the herpes virus, Epstein-barr, triggered  the estrogen receptor tumors of breast cancer than the HPV virus must represent the trigger of the other type of tumor.  What receptor does HPV use?  Non-melanoma skin cancer has also been associated with HPV where increased cannabinoid receptors have been found. The increased expression of cannabinoid receptors on non-estrogen-receptor breast cancer tumors could be easily validated.

 Let's look at bone cancers.  Each type of bone cancer has already been associated with a specific virus.  Ewings has been associated with CMV and Epstein barr. Interestingly Ewings has also been associated with the hormone swings of pregnancy which would elevate estrogen levels.  Chondrosarcoma has also been associated with estrogen receptors but as a bone cancer of the facial region the prime suspect should be herpes simplex one.

 Osteosarcomas  have  different receptors over-expressed on the surface, the IGF receptors and somatostatin receptors.  Osteosarcoms are the most common type and largest group of bone cancer which might infer that it is caused by more than one virus.  Hepatitis B is the polyomavirus which is similar to the JC virus, mouse polyoma virus, the rous sarcoma virus of chickens, sv40, and the murine FBJ virus. When these types of viruses infect cells IFG or somatostatins receptors increase.  An overlap exists with these 2 types of receptors.

Spindle cell sarcoma has already been documented and accepted to be caused by the RSV. The fact we can see a possible pattern, association of a virus, with each type of bone cancer is suggestive.

Looking at bone marrow cancers, benzene typically settles into the marrow, we find 2 virus families and 2 types of cancers originating there.  The flavivirus family which can infect the marrow has strong correlations with leukemia.  The herpes family viruses particularly epstein barr has correlations with lymphomas. Note that PAH carcinogens, like that found in tattoos, tend to move not just to bone marrow but the the closest lymph gland.

If we look at prostate cancer we find 2 types.  An estrogen receptor form triggered by a herpes virus and melanocortin receptor form. What virus uses the melanocortin receptor? The flavivirus called chikungunya virus has been isolated from prostate tumors. Prostate cancer patients have an increased risk of melanoma, skin cancer.  Melanoma cells over express melanocortin receptors too. Interestingly most people who have been bitten by a mosquito carrying west nile or other flaviviruses do not realize they are infected.  Flaviviruses could be the cause melanoma.

How about pancreatic cancer? There are 2 types of pancreatic cancer, exocrine and endocrine. Exocrine pancreatic cancers might involve nicotinic acetylcholine receptors since they are involved with digestive juice secretion. Enteroviruses might be using acetylcholine receptors to infect based on their association with acute flaccid paralysis and acetylcholine secretion. Coxsackie, an enterovirus, has already been linked to type one autoimmune diabetes and is the most likely culprit for pancreatic infection triggering exocrine pancreatic cancer.

 Looking at the endocrine tumors they appear to be over expressing dopamine receptors on their surfaces. The flu virus which has also been accused of trigger type one diabetes seems to be using the dopamine receptors. Think of parkinson's disease, dopamine receptors and the link of the flu virus triggering that autoimmune disease.  If a carcinogen was present during a flu infection one could end up with endocrine pancreatic cancer.  If these viral receptor associations are correct.

There is not enough evidence to prove that cancers wear the receptors that the viruses used to infect them but there is enough to investigate the possibility. With luck this will prove Co-carcinogenesis and we can prevent cancer with vaccines. Assuming we figure out how to make vaccines for all of these viruses.  One can only hope.

1. Prasanna Kumar, Fredrick A. Murphy. Francis Peyton Rous Emerg Infect Dis 2013 Apr; 19(4): 660-663
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647430/

2. Haverkos HW. Viruses, chemicals, and co-carcinogenesis. Oncogene. 2004 Aug 23; 23(38);6492-9
http://www.ncbi.nlm.nih.gov/pubmed/15322520

3. Francis Peyton Rous
http://www.encyclopedia.com/topic/Francis_Peyton_Rous.aspx

4.Chemical interactions with herpes simplex 2 virus: enhancement of transformation by selected chemical carcinogens and pro-carcinogens. Carcinogenesis 1982;3(10):1235-40

http://www.ncbi.nlm.nih.gov/pubmed/6293737

5. Epstein-Barr virus and telomerase: from cell immortalization to therapy. Infectious Agents and Cancer 2014, 9:8 http://www.infectagentscancer.com/content/9/1/8

6. HSV-1 remodels the host telomeres to facilitate viral Replication. Deng et al., 2014, Cell Reports 9, 2263–2278
http://www.cell.com/cell-reports/pdf/S2211-1247(14)00973-5.pdf

7. The inhibition of mitochondrial DNA replication in vitro by the metabolites of Benzene, hydroquinone and p-benzoquione. Chem Biol Interact 1985 may; 53(3):327-50
 http://www.ncbi.nlm.nih.gov/pubmed/4006011

8. Inhibitory effect of benzene metabolites on nuclear DNA synthesis in bone marrow cells. j. Toxicol Environ Health. 1989;26(3);277-91
http://www.ncbi.nlm.nih.gov/pubmed/2926830

9. Viral polymerases Adv Exp Med Biolo 2012; 726: 267-304
 http://www.ncbi.nlm.nih.gov/pubmed/22297518

10.Viruses and human breast cancer.  Future Microbiol 2006 Jun;1(1):33-51
http://www.ncbi.nlm.nih.gov/pubmed/17661684

Human papilloma virus is associated with breast cancer Br J Cancer 2009 Oct 20; 101(8):1345-1350
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737128/

Treatment of estrogen receptor positive breast cancer. Curr Med Chen 2013; 20(5):596-604

http://www.ncbi.nlm.nih.gov/pubmed/23278394

Cannabinoids, endocannabinoids, and cancer
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366283/

Cannnabinoid receptors as a novel target for the treatment of prostate cancer
http://cancerres.aacrjournals.org/content/65/5/1635.full

Cope JU A viral etiology for Ewing's sarcoma. Med hypotheses 200 Nov; 55(5):369-72
http://www.ncbi.nlm.nih.gov/pubmed/11058415

Kebudi R, Bilgic B, Gorgun O, Avan I, Demirvont M. Is the Epstein Barr virus implicated in Ewing sarcoma? Med Pediatr Oncol 2003 Apr; 40(4):256-7
http://www.ncbi.nlm.nih.gov/pubmed/12555258

Dubois SG, Perez-Atayde AR, McLean TW, Grier HE. J Pediatr Hematol Onco. 2008 Sep; 30(9)' 716-8 Late recurrence of ewing sarcoma during pregnancy: a report of 2 cases.

http://www.ncbi.nlm.nih.gov/pubmed/18776769

Chondrosarcoma and estrogen receptors

http://www.ncbi.nlm.nih.gov/pubmed/18203781

Chordoma and herpes

http://www.ncbi.nlm.nih.gov/pubmed/9177973

Chordoma and estrogen receptors

http://www.ncbi.nlm.nih.gov/pubmed/11131982

Rous P.  J Exp Med 1911 Apr 1;13(4):397-411 A sarcoma of the fowl transmissible by an agent separable from the tumor cells. 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213042/#bib2

Palmer JS, Duffy DL, Box NF, Aitken JF, O'Gorman LE, Green AC, Hayward NK, Martin NG, Sturm RA.  Melanocortin-1  receptor polymorphisms and risk of melanoma: is the association explained solely by pigmentation phenotype? Am J Hum Genet 2000 Jan; 66(1):176-86
http://www.ncbi.nlm.nih.gov/pubmed/10631149

Aiken WD, Anzinger JJ Case Rep Urol 2015 :120535 Chikungunya virus Infection and Acute Elevation of Serum Prostate-specific Antigen.

http://www.ncbi.nlm.nih.gov/pubmed/26167328

Hafiz S, Dennis JC, Schwartz D, Judd R, Tao YX, Khazal K, Akingbemi B, Mo XL, Abdel-Mageed AB, Morrison E, Mansour M. Int J Oncol 2012 Oct; 41(4):1373-80 Expression of melanocrotin receptors in human prostate cancer cell lines: MC2R activations increases prostate cancer cell proliferation.

http://www.ncbi.nlm.nih.gov/pubmed/22842514

Testicular cancer and Co-carcinogenesis

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 nobel prize)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen with a benzene ring inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications.

Testicular cancer can be linked to herpes simplex 2. (herpes appears to use estrogen receptors)

Estrogen seems to stimulate testicular cancer
http://www.ncbi.nlm.nih.gov/pubmed/14555521

Herpes simplex 2 found in testicular cancer patients
http://www.ncbi.nlm.nih.gov/pubmed/8397088

Is prostate and testicular cancer linked?
http://www.asco.org/press-center/men-who-have-had-testicular-cancer-are-more-likely-develop-prostate-cancer-although

One form of prostate cancer is triggered by herpes 2.

Herpes virus 2 and prostate cancer
http://www.practiceupdate.com/content/genital-herpes-may-double-prostate-cancer-risk/13075

Estrogen receptors and prostate cancer (assuming herpes uses estrogen)
http://onlinelibrary.wiley.com/doi/10.1002/pros.10242/abstract

Lung cancer and Co-carcinogenesis

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 nobel prize)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen with a benzene ring inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications.

Types of lung cancer (can we match a virus to each type?)

non-small cell carcinoma (85%) there are 3 types:

Squamous cell
adenocarcinoma
Large cell carcinoma


Small cell cancer? oat cell cancer? what virus is connected to this one? EBV?

scleroderma and small cell lung cancer
http://onlinelibrary.wiley.com/doi/10.1002/jso.2930290109/abstract
https://www.ncbi.nlm.nih.gov/pubmed/2841907
https://www.ncbi.nlm.nih.gov/pubmed/15897643

Cannabinoid receptors and non-small cell lung carcinoma?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025486/
http://www.ncbi.nlm.nih.gov/pubmed/21097714

Cannibus reduces tumors in 50% of common lung cancer
https://patients4medicalmarijuana.wordpress.com/marijuana-info/marijuana-and-your-lungs-recent-studies/

Squamous cell and HPV (HPV uses cannabinoid receptors..HPV?)
http://www.oncologynurseadvisor.com/headlines/hpv-infection-lung-cancer-risk/article/378102/

Squamous lung cells moved to breast (HPV also infects the breast)
http://www.ncbi.nlm.nih.gov/pubmed/18505069

Adenocarcinomas and adenosine receptors
http://www.ncbi.nlm.nih.gov/pubmed/23917542

adenoviruses are 10% of lung infections and have been found in adenocarcinomas
http://www.cancerbiomed.org/index.php/cocr/article/view/157

So what virus causes large cell carcinoma? Flaviviruses?

Large cell carcinomas and neuroendocrine tumors
http://journals.lww.com/ajsp/Abstract/1991/06000/Neuroendocrine_Tumors_of_the_Lung_With_Proposed.3.aspx

melanocortin receptors and neuroendocrine cells of brain (until i find a better reference)
http://www.ncbi.nlm.nih.gov/pubmed/7854347

Melanocortin receptors  and lung cancer
http://www.ncbi.nlm.nih.gov/pubmed/22147647
Lewis lung carcinoma
https://en.wikipedia.org/wiki/Lewis_lung_carcinoma

Logically this means some cancers are linked by viruses.
Large cell lung, melanoma, prostate...flaviviruses
Breast, cervical, squamous....HPV

How does co- Carcinogenesis explain anti-depressants, blood thinners, and glioblastomas consuming themselves?

 Recently in the news cancer cells, specifically glioblastomas, were found to be self-destructive with anti-depressants and blood thinners.
http://www.sciencedaily.com/releases/2015/09/150924142514.htm

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 nobel prize)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen with a benzene ring inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.


Glioblastomas have several virus culprits: hhv6, cmv, sv40, and jcv

HHV6 and CMV seem to use estrogen receptors to infect cells. (these might not be sensitive to the blood thinner treatment)

SV40 and JCV (simian virus and human polyoavirus) seem to use serotonin receptors.
These viruses are in the same family.

JCV and serotonin
http://www.ncbi.nlm.nih.gov/pubmed/19703243
serotonin inhibitors and block JCV infections

SV40 and serotonin
http://www.ncbi.nlm.nih.gov/pubmed/3022874
transgenic mice infected with sv40 have increased serotonin receptors

JCV, SV40 and BK virus are highly homologous viruses (related and similar)

Are these glioblastomas in the experiment sensitive to anti-depressants because started by JCV or SV40 use serotonin receptors?

serotonin receptors and anti-depressants (do they act like inhibitors ?)
http://www.ncbi.nlm.nih.gov/pubmed/21256009

What about the anti-depressants? The affect was a synergy between anti-depressants and blood thinners.

If telomeres have a central role in cancer is it possible blood thinners act on them?

Cycloastragenol was shown to stimulate telomere growth in 2009 (nobel prize)
http://www.luxivi.com/inform/7.html

Cycloastragenol was a chinese herb known to increase blood flow.

So the anti-depressants interfere with the virus at the receptor while the blood thinners are interfering with the viral telomere binding proteins?

When this came out I had mentally lumped ginko and cinnamon with it. Cinnamon and ginko both had life extentending properties and some suggested they had cancer protective abilities.  Why know one could pin point.  Both cinnamon and gingko seemed to be blood thinners too.

Gingko and rat's lifespan
http://www.ergo-log.com/ginkgolifespan.html

Cinnamon and worm's lifespan
http://www.life-enhancement.com/magazine/article/2285-cinnamon-extends-lifespan

Gingko is currently being examined for telomere lengthening
http://www.ncbi.nlm.nih.gov/pubmed/17312453

This might even be visable in the Gingko tree itself
http://www.ncbi.nlm.nih.gov/pubmed/20842436

Can medical blood thinners be acting on telomeres too?
Can simple cinnamon be lengthening telomeres?

What needs to be tested out:

Do other types of cancers with different virus triggers and different receptors fit this pattern? Can you put blood thinners with estrogen receptors inhibitors with  breast cancer cells and see the same self destruction of cancer? Is it a matter of selecting the right receptor?  At the same time? why do the drugs act together?

 Does cinnamon have an effect on telomeres? Can cinnamon replace the blood thinners in these experiments?

Brain Cancers and the Co-Carcinogenesis hypothesis

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer.

CMV (HHV5) and glioblastoma multiforme infection of glial cells
http://www.med.wisc.edu/news-events/new-evidence-links-virus-to-brain-cancer/32922
http://www.ncbi.nlm.nih.gov/pubmed/25699229

Craniopharyngioma and the herpes virus simplex (HHV2) infection of pituitary gland
http://www.ncbi.nlm.nih.gov/pubmed/18976107
http://www.ncbi.nlm.nih.gov/pubmed/8906037

Head and neck cancers and Epstein-barr virus (HHV 4) infection of squamous cells
http://www.infectagentscancer.com/content/pdf/1750-9378-8-7.pdf

The estrogen receptor of nerves cycles to the mitochondria but the estrogen receptors of adrenal cells like squamous cells cycle to the nucleus. Thus in nerves herpes breaks the mitochondria power house while in adrenal cells it destroys the nuclear cookbook.

Alzheimer's is herpes simplex (HHV1) infecting of the mitochondria of nerves thus destroying the nerves.
http://journal.frontiersin.org/article/10.3389/fnagi.2014.00202/full

Note that the virus alone does not cause cancer and that it needs a carcinogen. Co-carcinogenesis says both are needed.

 Imagine a virus as initially causing the DNA to replicate forever for it's own benefit.  Now imagine benzene which binds polymerases haulting copies.  Viruses have their own polymerases. Now imagine the carcinogen binds the viral polymerases better than the hosts.  So you have the cookbook of DNA open and no viral polymerase to compete with.

So what carcinogen gets into our brain?