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Post by lilsissy on Dec 27, 2009 20:11:05 GMT -5
I truly hate what I am about to write . I am seeing some stong connections between X.M.R.V. and Morgellons. XMRV has been linked to Chronic Fatigue /Fibromyalagia and Cancer. We have certainly have had Cancer related deaths and also many of us have Chronic/Fatigue and Fibromyligia. In investigating this XMRV I have noticed many simularities. I have noticed many of us carry very high VIRAL LOADS, HERPES and EPSTEIN BARR. X.M.R.V. shuts down the bodies response to viruses. It is indeed a very stange virus itself. I wonder is Morgellons, C.F., Fibro and Cancer....... a by-product of an unintended Agrobacterium mediation that was intended for plants? I know that my family also carries a 1q42 mutation with Kartengers Syndrome , because my daughters heart and chest organs are reversed . I do not know for sure exactly how this fits in but I think many of us on this board have this gene mutation spot. It is a spot that has a gap that allows for a gene insertion to be put in . I believe it is the most common and biggest naturally occuring gap area in the Human genome. It allows for the insertion of added genes. It is called Trisomy , a third gene , an added gene. You can not tell by looking at my daughter she is beautifull and very very smart. Some children born this way appear retarded some do not. This area 1q42 with Kartengers syndrome often results in a incomplete form of cystic Fibrosis when it is not fully displayed in carriers of that gene . I am a carrier , being the mother of this daughter and my sister also has situs abnormalities, this gene runs in the family. This would explain why we have trouble with Agrobacteium infections to begin with. Agrobacterium is know to be an infection in Cystic Fibrosis Patients. 1 in 25 people are silent carriers of this gene mutation for cystic fibrosis . In studing this gene mutation , the 1Q42 area , I also found that it is the same area responsible for early-onset Prostate cancer. I think this is just too much to be a co-incident, I believe more than ever Morgellons sufferers have an added gene mutation in the area of 1q42 which may be the result of an agrobacterium infections and / or makes us more susceptable to agrobacterium infections thus High Viral Loads and Cancer. This virus XMRV is also implicated in prostate cancer. So somehow 1q42 with Kartengers and X.M.R.V. are in connection with one another. Off the top of my head the both have added genes in this gap area. XMRV was discovered by laboratories led by Joseph DeRisi at the University of California, San Francisco, and Robert Silverman and Eric Klein of the Cleveland Clinic. Silverman had previously cloned and investigated the enzyme ribonuclease L (RNase L), part of the cell’s natural defense against viruses. When activated, RNase L degrades cellular and viral RNA to halt viral replication. In 2002, the “hereditary prostate cancer 1” locus (HPC1) was mapped to the RNase L gene, implicating it in the development of prostate cancer.[5] The cancer-associated “R462Q” mutation results in a glutamine instead of an arginine at position 462 of the RNase L enzyme, reducing its catalytic activity. A man with two copies of this mutation has twice the risk of prostate cancer; one copy raises the risk by 50%.[2] Prostate Cancer May Be Linked to Virus - RNASEL Gene Defends against Viruses February 24th 2006 Comon Flu Viruses Researchers at the Cleveland Clinic and the University of California San Francisco have identified a new virus in human prostate tumors. They are not sure whether this virus is linked to prostate cancer yet. The virus was found more often in human prostate tumors with two copies of the RNASEL gene mutation than in tumors with at least one normal copy of the gene, Forbes reported. Dr. Eric Klein said "This is a virus that has never been seen in humans before. This is consistent with previous epidemiologic and genetic research that has suggested that prostate cancer may result from chronic inflammation, perhaps as a response to infection." Dr. Klein is head of urologic oncology at the Cleveland Clinic's Glickman Urologic Institute. The researchers say that RNASEL is a gene that serves as an important defense against viruses. Scientists have suspected that this gene mutation and virus may be responsible for some types of cancer. The scientists used a new “virus chip” to identify the virus. This chip was used three years ago to confirm the identity of the SARS virus. Klein says this finding validates the use of the virus chip to discover previously unknown viruses. This may help us learn more about viral causes of disease. There are other cancers that may be caused or related to viruses. Liver and cervical cancer could be caused by a virus. Now scientists are investigating whether diseases may play an important role alongside genetics in causing breast, stomach and several other forms of cancer. There are environmental concerns as well. Future treatments and possible preventative measures may include enzymes that help kill invading viruses. Virus-Induced Gene Silencing, a Post Transcriptional Gene ...by U Turgay - 2009 - Cited by 1 - Related articles - All 9 versions Virus-induced gene silencing (VIGS) is one of the reverse genetics tools for ... an RNAse-like enzyme, are then incorporated into RNA-induced silencing .... The TRV silencing in plants is usually mediated by Agrobacterium tumefaciens. ..... virus-induced gene silencing in chili pepper (Capsicum annuum L. cv. ... www.hindawi.com/journals/ijpg/2009/198680.html - Cached US Patent 5589625 - Transgenic plants displaying multiple virus resistance and a process for their production US Patent Issued on December 31, 1996 Estimated Patent Expiration Date: January 18, 2015Estimated Expiration Date is calculated based on simple USPTO term provisions. It does not account for terminal disclaimers, term adjustments, failure to pay maintenance fees, or other factors which might affect the term of a patent. Abstract Claims Description Full Text View Patent Images (PDF) (Registered users only) Description BACKGROUND OF THE INVENTION 1. Field of the Invention This invention relates to transgenic plants that are genetically engineered to contain a DNA sequence encoding at least one polypeptide having a 2,5A synthetase activity thereby providing to said plants resistance against multiple taxonomic virus types. Moreover, this invention relates to a process for the production of said transgenic plants and to the use of said genetically engineered DNA sequence. 2. Description of Related Art Several methods for the construction of virus resistant plants are described in the state of the art. Genetically engineered resistance to a number of plant viruses has been reported by expressing coat protein of a respective plant virus in transgenic plants (Beachy, et al., Annu. Rev. Phytopathol., 28:451-474, 1990). A substantial virus-resistance to several plant viruses has also been demonstrated by expression of specific viral antisense RNA in transgenic plants (Cuozzo, et al, Bio/Technology, 6:549-557 1988; Hemenway, et al., EMBO J., 7: 1273-1280, 1988). The viral antisense RNA exhibits its function either by hybridizing to specific viral DNA or RNA sequences and thus blocking further reactions which are important for the virus propagation, or by ribozyme activity which results in a specific cleavage of viral RNA upon hybridization to said viral RNA. I am still working on this theroy and how it all fits together but it does seem unforutanly does seem to fit together.Notice this chip, hmmmmmm Jen Will it tell us of added genes ? Jen
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Post by lilsissy on Dec 27, 2009 20:18:30 GMT -5
much research is going on into X.M.R.V. check this out,
Friday, November 27, 2009 The Modus Operandi: Part II In my previous post, I gave my theory explaining the female predominance of ME/CFS and fibromyalgia, in this post I will explain my theory behind the neurological symptoms of ME/CFS, FM, and Autism. My theory centers around the SYG1 membrane protein, which has been identified as a synaptic guidepost, directing neurons to connect to each other. The SYG1 protein is in the immunoglobulin superfamily, with an extracellular domain, a single transmembrane segment, and an intracellular loop. SYG1 binds to its receptor SYG2, which is also a member of the immunoglobulin superfamily. Ironically, SYG1 is most heavily expressed during fetal development and early childhood, and its expression greatly diminishes thereafter. In adulthood, it continues to be expressed in the limic region (which includes the hypothalamus), at neuromuscular junctions in skeletal muscle, and in arterial walls. When it is activated, it initiates selective synapse elination through the SCF-Ubiquitin ligase complex - when it works properly, SYG1 binds to SKR, inhibiting formation of the SCF complex (Skp1-cullin-F-Box complex), protecting nearby synapses.
It is my opinion that SYG1 dysregulation is directly correlated to symptoms noted in all three conditions: ME/CFS, FMS, and Autism. If you disrupt proper synapse formation in early childhood development, you almost certainly will end up with a developmental disability. It leads me to theorize as some have that XMRV is passed from mother to child through saliva, body fluids, breast milk, and quite possibly placental transmission. Likely the process of autism begins well before the first symptoms appear, and with XMRV screening could be reversed by early use of antiretrovirals, either by treating an infected mother, or the child. There has been some mention by Dr. Mikovits that vaccines could create the immune insult setting off autism, however I believe the risk is far, far smaller than the immune insult from getting sick - as you are only exposed to an antigen at a point in time, as opposed to receiving a continuous onslaught of viral antigen while the immune system clears the virus.
Another interesting point is that SYG1 is primarily expressed in slow sodium fibers in the peripheral nervous system at neuromuscular junctions- nerve fibers responsible for transmission of pain signals - leading to an amplified pain response. Substance P opens slow sodium channels, and closes potassium channels - and if you've got uncontrolled synapse formation, it may very well explain some of the observations made in FMS.
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Post by rafael25 on Dec 27, 2009 23:21:59 GMT -5
Hello Everyone!
I have suffered with Chronic Fatigue, Multiple Chemical Sensitivities, Allergies and allergic reactions that drove me to the edge of seizures, symptoms that look a lot like Restless leg, symptoms to hepatitis, symptoms of lupus, insomnia, migraines, and much more.
After three years into the Chronic Fatigue with the Fibro pain that comes on and off, I think that Chronic Fatigue is related to the way in which people think. I do not mean is psychiatric like a chemical unbalance, a 'mental' condition, nor brain injury. I do not say it is hipocondria. I mean that the sufferer's thought process at the logical level is adulterate , or corrupt. I do not mean that the patient's thought are morally wrong or corrupt as far as wanting something outside of what good or perfect. I mean that there is like a veil or lens in their perception that is taking the image of reality and giving it twists and disturbances that they are not really there.
I give you an example with optics: The reality of a healthy person is like looking one self in a mirror. We can see ourselves with realistic proportions and dimensions. The person with Fibro or CFS sees itself in a mirror but in a mirror of a 'Fun House' attraction. When he/she looks everything looks familiar but everything is changed in proportion. You know, one looks too tall, too wide, too short, because of the undulations in the mirrors. The mirrors don't reflect reality with perfect veracity. So in the same way, the patient is not really being truthful to his/her inner core. His/her own mind has a way to derail the energy that should be flowing from the person's life force- because every time the person acts, his thought process can not determine if the person is accepting or rejecting his own will and conscience. The patient does not know if her own conscience is her friend or her foe. Something really interior- something that I can't describe in the nervous system simply tries to press the 'turn off button'. Imagine that a computer would turn itself off when it becomes self- conscious that it is acting under the influence of a dangerous virus. So I think that the human body works similarly. When the body/mind detects that he/she is not acting for his own benefit and welfare, it shuts down.
Fear and anxiety are always linked to CFS and FM. I have being able to retrieve many documents on Oriental Medicine- and yes, the pain and muscle weakness- the vacuity of one's body is always linked to fear and anxiety. Also the desire for being perfect and to be accepted. I trace feelings to human interaction and specially to intra-family relations. One has to deprogram oneself from so much stuff- I could call it 'negativity', or 'prejudice' but that is a terrible oversimplification. CFS is in my opinion related to emotional slavery. It comes to the point that the patient is simply lost in time and space. It is the people and the places around the patient which give her a sense of grounding, not her own mind.
These are my two cents.
Peace!
Mar.
ps: So the problem is in perception, as the patient can not discern times in which compromises shall be made.
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Post by lilsissy on Dec 28, 2009 0:22:31 GMT -5
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Post by rafael25 on Dec 28, 2009 1:08:11 GMT -5
Lilsissy, Dear, I think you brought in a good point. Sickness can change moods. This I have heard from doctors. But what if it also works the other way around? What if emotional states can debilitate one's immune system so that the patient might become more susceptible to infections from pathogens that would be otherwise classified as innocuous? What was first, the chicken or the egg? I can tell you that once the body starts to find itself crippled the mind decides that it is time for a change...hmmm how suspicious. Is the patient 'adapting' to the sickness, or is the patient showing his true self or true conviction in times of crisis, or is the patient letting go off his own security blanket, fake behavior, doormat complex? I used to be a real doormat. I had no direction! The moment I found myself crippled I became a real pain. I could not tell if I went from all doormat to all so demanding- but it took me years to figure out that I needed and continue to need balance, in all things and all situations. I was never sincere to my own thoughts, desires, and feelings- so when I was 'dying', I felt like I had been cheated from 'my life'. The life that I never built- because I was fearful and/or pretending to be self-satisfied. I was not angry with anyone, I did not feel vengeful, but I could not agree nor trust people. I knew that there was something very sketchy with the world, and this whole societal system and all the technological mombo jumbo that we have built around it is kinda tampering with the truth. We do not know the truth and no one minds to bring it up because we can numb the pain. So now, I search for myself every moment. I am not searching for myself out in some fixed point in the imaginary future. I do not search for myself in my past. I search for myself here in the present moment. This has to be independent of the intemperate love or passions that we feel for family, friends, and love ones. This has to be beyond all grievances and past conflicts. We have to be aware that our bodies are a miracle! We have to live in our flesh- and truly accept our flesh, and try to understand it- not just try to numb it. If we silence our flesh, it tries to speak louder through sickness. Now you guys know my heart . More later. Peace, Mar.
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Post by aqt on Dec 28, 2009 11:08:02 GMT -5
Dearest raphael,
You know how I am. I must add my two cents as well...here it goes
I was born sick in 1968. I was born with the culmination of the mycoplasma infections that both of my parents were infected with.
As a child, I recieved mandatory vaccinations which "triggered the mycoplasma" and I become more ill
As I grew up, I also contracted my own forms of mycoplasma through insect bites.
I then became a nurse and lined up for every vaccination offered. After all, the CDC said I should and the FDA had approved it.
More vaccines to trigger more mycoplasma...all the time, delpleting my immunity and causing cytokine storming.
Then comes the Morgellon's to really mix things up and get the party started.
I had always had a very positive outlook on life...until I became so ill that it was difficult to function as a human being.
In the process of my illness, fear and anxiety were "triggered" in me as well....as I learned through my BioSET treatments.
I believe the illness causes the fear and anxiety within us, changing our state of mind.
Before I became deathly ill, I was outgoing, energetic, funloving kind of gal.....
when I became ill, I became a monster.
Now that I am well and balanced and healthy and happy (which you wished for me long ago, if you remember correctly)
I am back to my "old" self again and it is wonderful
I am so blessed and you my friend are one of my biggest!!!!
with love and adoration,
my two cents ;D
aqt
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Post by skyship on Dec 28, 2009 23:16:22 GMT -5
A replication-defective murine sarcoma virus (sarcoma viruses, murine) isolated from a rhabdomyosarcoma by moloney in 1966. rhabdomyosarcoma can get from gadolinium dye contrasts for MRI. www.mridoc.com/cases/msk/002.html==================== Organization of Murine Sarcoma Virus Genomes Excerpt Moloney murine sarcoma virus (M-MuSV) is a murine retrovirus of hybrid genetic origin. M-MuSV was isolated as a novel sarcomagenic agent following passage of Moloney murine leukemia virus (M-MuLV) through a Balb/c mouse (Moloney 1966). The new MuSV differed from the leukemia virus in three important respects: (1) MuSV could induce focal transformation of fibroblast monolayers in vitro, whereas MuLV had no effect on fibroblast phenotype in vitro; (2) MuSV could induce fibrosarcomas in vivo; and (3) MuSV was replication defective, being unable to specify proteins required for its own replication. Because of the latter condition, M-MuSV requires coinfection by a competent helper virus (e.g., an MuLV) in order to replicate. The genome of M-MuSV was seen to derive largely from different portions of M-MuLV (Dina et al. 1976; Hu et al. 1977). An exception to this is a region of about 1.2 kb that is homologous with sequences present... symposium.cshlp.org/content/44/721.extract============ this is an RNA virus not a DNA virus, but it tracks into dna....... seems there was a defect in the construction of it, and the rous is related to avian virus. ============ Characterization of Virus-specified Proteins Present in NRK Cells Infected with a Temperature-sensitive Transformation Mutant of Moloney Murine Sarcoma Virus 1. T. G. Wood, 2. J. Peltier-Horn, 3. W. G. Robey*, 4. D. G. Blair*, and 5. R. B. Arlinghaus + Author Affiliations 1. Department of Biology, The University of Texas System Cancer Center, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77030; *Laboratory of Viral Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205 This extract was created in the absence of an abstract. Excerpt The nondefective mammalian type-C retrovirus genome contains a single-stranded polyadenylated RNA molecule about 9–10 kb long, which consists of at least three genetic regions (Baltimore 1975). These include the gag gene, which is located near the 5′ terminus of the viral genome and which encodes the internal structural proteins of the virus (Jamjoom et al. 1977; Murphy and Arlinghaus 1978), the pol gene, which codes for the viral reverse transcriptase (Kopchick et al. 1978, 1979; Murphy et al. 1978), and the env gene, which is located near the 3′ terminus of the genome (Rothenberg et al. 1978) and which encodes the proteins of the viral envelope (Karshin et al. 1977). Viruses of this group replicate in, but cause no morphological alteration of, cells in culture; they induce neoplastic diseases in vivo only after extended latent periods (Aaronson and Stephenson 1976). symposium.cshlp.org/content/44/747.extractso we are looking at gag, pol and env genes: gag: holy moloney: after AIDS and HTLV came the XMRV in full embodiment. A Primer on XMRV XMRV is a retrovirus - a virus that uses its RNA to copy its genetic material into host DNA. The best known retrovirus is HIV (Human Immunodeficiency virus) - the virus that causes AIDS. XMRV is only the third such retrovirus discovered to infect humans, after the discovery of HTLV. Like HIV, XMRV has 3 genes in common - gag, pol, and env. The gag gene encodes the capsid and matrix proteins, the pol gene encodes a single protein which is cleaved into three separate proteins by the viral protease - reverse transcriptase, viral protease, and integrase, and the env gene encodes the envelope glycoproteins. The XMRV also contains an androgen response element gene, which I will discuss a theoretical role in a future post. The XMRV genome is somewhat smaller than the HIV genome - 8161 base pairs as opposed to ~9500 base pairs in the HIV genome. Based on initial findings, it appears that XMRV infects the immune system in ways that are all too familiar in HIV. The envelope glycoproteins likely bind to some yet unknown immune system protein like HIV binds to the CD4 receptor, and co-receptor, possibly CD8, CD 16 or CD 56 on the surface of NK cells. so env is the glycoproteins..................way to familiar in HIV? so this acts like aids, downs the immune system, on surface of NK cells. natural killer cells, kills viruses, but in this case doesn't. here is what it looks like: ======================== www.thelatestnews.in/xmrv-found-in-human-prostate-cancer-cells/18511.html"The results of a recent research study led the researchers from the University of Utah and Columbia University medical schools shocked to find traces of XMRV virus in human prostate cancer cells. XMRV found in human prostate cancer cells XMRV (Xenotropic murine leukaemia virus-related virus) is known to cause leukemia and other tumors in animals. XMRV is a retrovirus like HIV which works by inserting a copy of its own DNA into the chromosomes of a cell they infect. Where this occurs next to a gene that regulates cell growth it can disrupt the normal development of the cell. They say it was associated with more aggressive tumors and found in only 6% of non-cancerous prostates. Dr Ila Singh, who led the study from the pathology department at the University of Utah, said: “We still don’t know that this virus causes cancer in people, but that is an important question we are going to investigate.” This is the first report to link XMRV to human cancers.'"..................... ================= Singh is dude going after the construction of this, and most likely will find the defects as are some others. relates back to typoid and avian viruses, men women in wwII given vaccines for this. or was part of a bioweapon used during war. ========== picture in all of it's ugliness: ================ tinyurl.com/yab95as4.bp.blogspot.com/_3mcPKxO-09w/StDWwqPz7zI/AAAAAAAAAd4/62d47nbA1KI/s1600-h/Prostate_Cancer_cell_ division__SEM_SPL_705590113.jpg skytroll
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Post by skyship on Dec 28, 2009 23:31:03 GMT -5
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Post by lilsissy on Dec 29, 2009 0:18:24 GMT -5
Great information there sky!
I need to chew on it for sure but the picture you posted shocked me, Someone posted a sample on Lymebusters that looked quite simular but it was brownish black. Will check.
Also think they will say it is somehow connected to the Dogs, virus . Vague on this though.
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Post by lilsissy on Dec 29, 2009 0:24:06 GMT -5
Also think this needs to be looked at , what would be the new assembly,
XMRV was discovered by laboratories led by Joseph DeRisi at the University of California, San Francisco, and Robert Silverman and Eric Klein of the Cleveland Clinic. Silverman had previously cloned and investigated the enzyme ribonuclease L (RNase L), part of the cell’s natural defense against viruses. When activated, RNase L degrades cellular and viral RNA to halt viral replication. In 2002, the “hereditary prostate cancer 1” locus (HPC1) was mapped to the RNase L gene, implicating it in the development of prostate cancer.[5] The cancer-associated “R462Q” mutation results in a glutamine instead of an arginine at position 462 of the RNase L enzyme, reducing its catalytic activity. A man with two copies of this mutation has twice the risk of prostate cancer; one copy raises the risk by 50%.[2]
So what could we do to fix it?
What resets D.N.A.? God Voacanga Afiricana Seeds (ibogaine) Bioset.
Jen
Bet they will try to sell us on verichip with virus sensor .
Yes , I do believe in the power of the mind, spirit . Most of all the Stripes by which we are healed.
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Post by aqt on Dec 30, 2009 16:49:21 GMT -5
lilsissy, I agree with the Iq42 concept....we Morgellonites have the "gap" in the genes which allows for the other genes to be inserted. If they used plant genes in the making of the morgs, we are now part plant....leaving us open to agrobacterium infections?? this is all so interesting...and "coincidental", isn't it? I self diagnosed CFS and Fibro and then... I was formally diagnosed with CFS and Fibro self diagnosed Morgellons ;D let's keep pluggin'...we're getting there!!! aqt
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Post by aqt on Dec 30, 2009 17:04:54 GMT -5
I also wanted to add that I believe the viruses may perhaps lay the ground work for Morgellons but the "fibers" in our environment and in our bodies have a certain "intelligence".
I think there is a culmination of things happening here
Immune systems damaged since birth through vaccines Immune system not repaired/genetically modified foods Immune system cannot detect retroviruses at all Immune system can't fight off other viral/bacterial infections Immune system evaded also by Morgellon's intelligent entity Immune response=protein fibers
jmho,
aqt
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Post by lilsissy on Jan 1, 2010 20:19:08 GMT -5
interesting, X.M.R.V. a part of swine flu?
Sunday, December 13 XMRV Virus Causes Chronic Disease Syndrome
Dr. Schimpff, former CEO of the University of Colorado Medical Center, has an interesting book on the future of medicine. He and I were coinvestigators on an Operation Room of the Future grant designed to upgrade information technology in the new surgery center the University opened a few years ago.
He also has a good blog with a recent posting on the XMRV virus. Frequency Foundation subscribers have already received the frequency set as part of the Swine Flu series. Most of you don't realize that XMRV is one of the many viruses that are part of what is called "Swine Flu" as conventional medicine has a tough time even confirming that you have the 1918 swine flu virus and doesn't determine what other organisms are making you sick. After you get the swine flu you will likely be chronically infected with XMRV unless the virus is eliminated with frequencies.
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Post by aqt on Jan 5, 2010 17:10:00 GMT -5
Breaking It down:
Definition of Xenotropic virus
Xenotropic virus: A virus that can grow in the cells of a species foreign to the normal host species, a species different from that which normally hosts it.
Xeno- means foreign while -tropic refers to growth. So xeno- + -tropic = capable of growing in a foreign environment.
so, they built the virus that could infect EVERYTHING
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Post by aqt on Jan 5, 2010 17:11:59 GMT -5
MURINE
1. belonging or pertaining to the Muridae, the family of rodents that includes the mice and rats. –noun. 2. a murine rodent
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Post by aqt on Jan 5, 2010 17:14:53 GMT -5
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Post by aqt on Jan 5, 2010 17:18:09 GMT -5
A retrovirus is an RNA virus that is replicated in a host cell via the enzyme reverse transcriptase to produce DNA from its RNA genome. The DNA is then incorporated into the host's genome by an integrase enzyme.
The virus thereafter replicates as part of the host cell's DNA.
Retroviruses are enveloped viruses that belong to the viral family Retroviridae.
The virus itself stores its nucleic acid in the form of a +mRNA (including the 5'cap and 3'PolyA inside the virion) genome and serves as a means of delivery of that genome into cells it targets as an obligate parasite, and constitutes the infection.
Once in the host's cell, the RNA strands undergo reverse transcription in the cytosol and are integrated into the host's genome, at which point the retroviral DNA is referred to as a provirus. It is difficult to detect the virus until it has infected the host.
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Post by aqt on Jan 5, 2010 17:26:45 GMT -5
So, we have a virus built to live in "foreign" environments, designed from a rat virus, throw in a little HTLV-1, related to Leukemia and design it as a "retro" virus...which has the ability to recombine with our RNA...which builds the DNA...and becomes integrated into the host's genome.wt?
not to mention the artificial intelligent polymer fibers being added to the mix through the use of Illegal Aerosol Operations recombining with human DNA collectively.
Perhaps only us with XMRV are the ones showing these bizarre symptoms?
and where do the hexagons come in?
So much in the mix....
aqt
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Post by aqt on Jan 5, 2010 17:40:33 GMT -5
Integrase is an enzyme produced by a retrovirus (such as HIV) that enables its genetic material to be integrated into the DNA of the infected cell. It is also produced by viruses containing double-stranded DNAs for the same purpose.It is a key component in the pre-integration complex pre-integration complex-The pre-integration complex (PIC) is generally composed of the viral genetic material and associated proteins (viral and host) after release into the cell. In HIV, this includes the viral core which surrounds the RNA. This complex is responsible for reverse transcription of the viral RNA genome into dsDNA and prepares it for retroviral integration into the host DNA within the nucleusen.wikipedia.org/wiki/Pre-integration_complex
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Post by skyship on Jan 6, 2010 0:52:41 GMT -5
There are the RNA viruses that seem to be related to this XMRV IPNV, Infectious Panreacreatic neecrosis virus, caused by RNA viruses as well. This involves up to 5 or more viruses. Reovirus, Andenovirus, and others.... Involves this: VP1 rna polymerase VP2 Core capsid Protein VP3 quanylytransferase VP1, 2, 3. is associated with CFS and XMRV and IPNV....Prostate cancer...and others. vp1: Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach. John K S Chia, Andrew Y Chia; J Clin Pathol 2007 "A total of 135/165 (82%) biopsy specimens stained positive for VP1 [an enteroviral protein] within parietal cells.... Taken together, the findings of enteroviral protein, RNA and the growth of non-cytopathic viruses in the stomach tissue of CFS patients, years after initial infection, suggest a strong association between enteroviral persistence/infection and CFS. [Note]: Enteroviruses cause acute respiratory and gastrointestinal infection, with well-documented tropism for the central nervous system, heart and muscles." www.name-us.org/ResearchPages/ResImmune.htm#2009------------ WOW..................guess HHS got CDC attention.........or ?...... Holmberg did! another hero............... ====================== HHS Coordinating Xenotropic Murine Leukemia Virus-Related Virus (XMRV) Scientific Activities The U.S. Department of Health and Human Services (HHS) has formed an interagency scientific working group on XMRV. The Blood XMRV Scientific Research Working Group will report to the Department’s Blood, Organ and Tissue Senior Executive Council through established mechanisms. No formal statement has been issued yet, but the working group includes representatives from the DHHS Office of Public Health and Science, the National Institutes of Health (NIH), the Centers for Disease Control and Prevention (CDC) and the Food and Drug Administration (FDA). The working group will have scientific responsibilities for investigation of XMRV as it relates to the blood supply and CFS. Suzanne D. Vernon, PhD, the CFIDS Association’s scientific director, has been asked to participate in the XMRV scientific working group. Dr. Jerry Holmberg Dr. Jerry Holmberg of the HHS Office of Public Health and Science made a brief presentation on Oct. 30, 2009 to the DHHS CFS Advisory Committee. He described the existing response systems that address threats to blood safety, such as new and emerging infectious agents like XMRV. The HHS Blood XMRV Scientific Research Working Group will be chaired by a representative of the NIH’s National Heart, Lung and Blood Institute (NHLBI) and will collaborate closely with the agencies in charge of these systems, including the NHLBI’s Retrovirus Epidemiology Donor Study (REDS). REDS was created in 1989 to address risks associated with HIV-1, HIV-2, HTLV-1 and HTLV-2 in the general blood supply. In more recent communications with Dr. Holmberg, he stated that the Blood XMRV Scientific Research Working Group is taking a three-stage approach to its handling of the issues related to XMRV and the possible link to human disease. The first stage will be to standardize and validate laboratory methods and reagents for XMRV testing. This is important since variations in sample collection and laboratory procedures can produce discrepant results. These standardized approaches will be used initially to test 1,200 healthy donors’ blood samples and 100 CFS patients’ blood samples collected by Dr. Judy Mikovits of the Whittemore Peterson Institute. Stage two will assess the prevalence of XMRV in the general population and blood supply, as well as in other CFS patient cohorts. The third stage will be a series of studies to understand how XMRV is transmitted, whether it causes human disease, and how it affects various subgroups of the population. The immediate focus is to ascertain any risks to the general blood supply that XMRV might pose, but the scientific working group is also addressing validation studies for diagnostic tests and if necessary, potential blood screening tests. If the studies indicate that screening is required for blood products, blood screening tests, must be submitted to and approved by the FDA before they can be marketed. Neither of the tests currently being offered by two commercial labs has been reviewed by the FDA. According to CDC, their studies using samples obtained from the Whittemore Peterson Institute have HHS attention. The Laboratory Branch in CDC’s Division of HIV/AIDS Prevention is doing the XMRV testing and not the CDC CFS research group in the Division of Viral and Rickettsial Diseases. Representatives from the FDA attended the XMRV meeting sponsored by Abbott Laboratories at Cleveland Clinic on Nov. 11, 2009. Dr. Robert Silverman of the Cleveland Clinic gave a seminar about XMRV for HHS staff on Dec. 2, 2009. Dr. Holmberg emphasizes the need for careful application of scientific methods to ensure that these studies are conducted with exceptionally high rigor and reliability so that the results provide a solid scientific foundation for moving forward. He understands the strong interest within the CFS patient community for swift action and definitive answers, and expressed the high priority that this subject is receiving within a broad range of functions within the Department of Health and Human Services. The CFIDS Association will provide updates on these important activities as new information becomes available. www.cfids.org/cfidslink/2009/120203.asp=========================== Makes one wonder if this is all involved in the many viruses used to mutate into A and B blood, is what causes many of these problems. I will see if there is a link XMRV and the A and B blood issues, also link of XMRV to IPNV. and the heart attacks happening, all related to blood issues. If the Kaiser/CDC crap don't work out, well we went in the back door, so did some others! Brave souls! skyship
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Post by skyship on Jan 6, 2010 1:55:50 GMT -5
Okay XMRV, (CFS) VP1 (found in CFS biopsies), VP1, 2 and 3 (found in IPNV, and) pancreas VRC (vanadyl ribonucleoside Complex)(linked to androgen receptor) Interaction of vanadyl ribonucleoside complex with the androgen receptor. Ohara-Nemoto Y, Yoshida M, Ota M. Department of Biochemistry, Iwate Medical University School of Dentistry, Japan. The addition of vanadyl ribonucleoside complex (VRC), a potent inhibitor of RNase, to the transformed 4.5S androgen receptor from rat submandibular gland caused an increase in the sedimentation coefficient to 7.0S. Moreover, VRC decreased the DNA-cellulose binding of the transformed receptor; 50% inhibition of the DNA-cellulose binding was achieved at 1.8 mM VRC. On the other hand, agents related to VRC and oxoanions of transient metals, such as ribonucleoside, vanadate, molybdate, tungstate and arsenate, exerted no effect on the DNA-cellulose binding ability of the receptor. These findings suggest that VRC binds to the transformed androgen receptor at the DNA-binding site and that both oxovanadium ion and ribonucleoside are indispensable for the binding of VRC to the transformed androgen receptor. www.ncbi.nlm.nih.gov/pubmed/3190719skyship
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Post by aqt on Jan 6, 2010 9:51:04 GMT -5
Found this: spumavirus A spumavirus or foamyvirus is a genus of the retroviridae family. Spumaviruses are exogenous viruses that have specific morphology with prominent surface spikes. The virions contain significant amounts of double-stranded full-length DNA, and assembly is rather unusual in these viruses. Normally, the envelope membrane is acquired by budding through the endoplasmic reticulum. However, in, for example, the equine foamy virus (EFV), budding from the cytoplasmic membrane occurs. en.wikipedia.org/wiki/Spumavirus
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