Cancer in and of itself is a virus by the best definition.
I am bit weary. How do auto immune diseases start then ?
This is wrong.
Is it ? By definition of behavior a cancer cell is basically a virus. It grows out of control and without purpose. A cancer cell is basically just a regular cell that has genetic flaw that cuase reproduction without need and cancer cells typically do not serve the function of the original cell. For all intensive purposes they are a virus like cell.
A virus does not grow. A virus has no organization. A virus has no purpose other than reproduction. Whereas cancer cells do. They grow, they organize themselves into structures reminiscent of some of those present in the human body, they perform other functions than just growth and division. Viruses are very small, on the scale of nanometers wide. Cells are typically around 1000x bigger. Viruses necessarily contain only a few pieces of nucleic acid and a protein coat, whereas cells contain so much more. Viruses require a host cell to replicate.Is it ? By definition of behavior a cancer cell is basically a virus. It grows out of control and without purpose. A cancer cell is basically just a regular cell that has genetic flaw that cuase reproduction without need and cancer cells typically do not serve the function of the original cell. For all intensive purposes they are a virus like cell.
A virus does not grow. A virus has no organization. A virus has no purpose other than reproduction. Whereas cancer cells do. They grow, they organize themselves into structures reminiscent of some of those present in the human body, they perform other functions than just growth and division. Viruses are very small, on the scale of nanometers wide. Cells are typically around 1000x bigger. Viruses necessarily contain only a few pieces of nucleic acid and a protein coat, whereas cells contain so much more. Viruses require a host cell to replicate.
Also, cancer cells have far more than a single genetic "flaw". Cells require several different cellular 'switches' to be deactivated before they can become cancerous. And along every step of the way, a precancerous cell is liable to be picked up by the immune system and destroyed. If getting cancer were as simple as you made out, none of us would survive birth.
Next time, I suggest you look up your words and make sure you know what they mean before saying something like this.
haha, okay you had me going for a while there, but now I know you're just trolling. Pretty good job, I must say.
edit: on the off chance you were serious, a virus is an infectious obligate intracellular parasite. Cancer doesn't fit that description. Eukaryotic cells are not viruses.
A virus isn't cancer. Cancer isn't a virus.your entirely to blinded by the "legalees " of the medical field to see it for what it is.
That's not quite true. It obviously depends on what you call 'meaningful', but adenocarcinomas, for example, form in gland-like structures, hence the name.no cancer grows with any meaningful structure.
No, they don't.BTW I am aware of the difference between a cancer and a virus. My point is that they behave in the same fashion.
That's not quite true. It obviously depends on what you call 'meaningful', but adenocarcinomas, for example, form in gland-like structures, hence the name.
No, they don't.
Yes they do.
admittedly in your own research they are finding virus fragments in cancer cells. Well one might ask
Why is that ?
so are cancer and virus's interelated ?
hmmmm.
Viruses can cause cancer, so yes, there is some relationship. This is well known and fully accepted science.
But they don't as you put it, "behave in the same fashion." It's like saying a great white shark is a hemorrhage. There is a causal relationship in some instances, but they are very different things.
without all the menusha.
define in as few words as possiable the behavior of
a virus
and a cancer
Thanx you so much for explianing what I was trying to get at.
When you get a vaccine fo say measales. We are giving Measales to the person being vaccinated. givin that the virus is genetically altered it no longer represents the actual virus in the wild. Ergo the vaccine will not be effective.
BTW getting the mseaes is a 100% effective guarentee against reinfection. Given the data on the measales vaccine that I have seen on and off over the years. the vaccine does not work with modern strains.
Also measales just isn't that bad. Really no worse then chicken pox excpet for the high fever. Which if left alone poses no significant threat. Mot of the complications with measales are cuaed by overly aggresive treatment altering the normal path of the bodys immune response.
Yes they do.
Next time you open your yapper consider that some people are completley clueless like me but don't know it.
I am a raving idtiot
I hesitate to say either "behaves."
Virus: Infectious, filterable particle.
Cancer: Non infectious, unregulated growth of host cells.
Well behavior is the hall mark of diagnosis.
Funny you call a virus a particle. Which it is not. usually it comes over in a cell nasal,oral etc as a host and the virus itself is the equivalent of a hacker. It hacks the host cell and alters the host cells behavior by changing the dna of the host cell.
Are cancers non infectious ? I would disagree with that statement. Provided with food and nutrition and they will infect the host and grow without purpose.
The only purpose either virus's or cancer have is continued reproduction.
So the behavior is the same.
Work from there how they might be interelated.
Wrong, wrong, sort of right, wrong, and you don't know what infectious means.
Wrong, wrong, sort of right, wrong, and you don't know what infectious means.
he is a troll. also trolling in most L&R Threads. just look at his post. -> ignore
Now scientists have found that the vitamin D receptor is a key player amid the gut bacteria - what scientists refer to matter-of-factly as the "gut flora" - helping to govern their activity, responding to their cues, and sometimes countering their presence. The work was published online recently in the American Journal of Pathology.
The findings deliver a new lead to scientists investigating how bacteria might play a role in the development of inflammatory bowel diseases such as Crohn's disease or ulceractive colitis. The work complements studies suggesting that Salmonella infection can increase the risk of inflammatory bowel disease.
"Vitamin D deficiency is a known factor in the pathology of inflammatory bowel disease and colon cancer," said microbiologist Jun Sun, Ph.D., of the University of Rochester Medical Center, "but there have been very few reports about how bacteria might play a role by targeting the vitamin D receptor. Our work suggests one possible mechanism, by working through the vitamin D receptor, a sensor and regulator for the majority of functions of vitamin D."
Sun specializes in the actions of bacteria in the body and how their interactions within the body contribute to disease. She has shown that bacteria often found in the human intestine affect molecular signals known to contribute to inflammatory response and cell growth.
Her work with the vitamin D receptor takes place at a time when the molecule is coming under increasing scrutiny. Scientists have associated vitamin D and the receptor with many types of cancer, as well as osteoporosis, heart disease, diabetes, inflammatory bowel disease, and infection.
Sun's team took a close look at the vitamin D receptor in mice and its interactions with bacteria in the colon. The team studied normal mice; mice in which the vitamin D receptor had been knocked out; and mice that were completely free of any germs. Scientists observed how the mice responded to infection with either a harmless strain of E. coli or a pathogenic strain of Salmonella Typhimurium.
The team found that Salmonella is able to regulate the vitamin D receptor, increasing its activity and determining where in the colon the receptor is active. In the presence of Salmonella, the receptor was more prevalent than usual deep within folded intestinal structures known as crypts.
Sun's team also discovered that the vitamin D receptor plays a key role in defending the body from assault by Salmonella and squelching inflammation. The receptor stops a molecule known as NF-Kappa B, a well-known master player in the world of inflammation, by binding to it and preventing it from activating other inflammatory molecules. While scientists have known that the receptor interacts with NF-Kappa B, details of the interaction modulated by bacteria in the colon are new.
The scientists found that Salmonella was much more virulent and aggressive in mice in which the vitamin D receptor had been turned off. These mice showed higher levels of activity of inflammatory molecules, and they lost weight more quickly and were much more likely to die in response to infection.
"We live together in a mutually beneficial state with most of the bacteria in our gut," said Sun, assistant professor in the Gastroenterology and Hepatology Division of the Department of Medicine. "They help us digest foods like fruits and vegetables, and we provide them a place to live and thrive. We co-exist peacefully - most of the time.
"But we aren't able to culture most of these bacteria in the laboratory, and we don't know what most of them are doing. We need to understand our gut flora much more than we do. This is particularly important for understanding how we might manipulate the natural gut flora to stop an invader like Salmonella," added Sun, who also has appointments in the James P. Wilmot Cancer Center and the Department of Microbiology and Immunology.
Salmonella (S.) is the genus name for a large number (over 2,500) of types of bacteria. Each type is distinctly identifiable by its specific protein coating. The types are otherwise closely related. Salmonella bacteria are rod-shaped, flagellated, Gram stain-negative, and are known to cause disease in humans, animals, and birds (especially poultry) worldwide.
The terminology that identifies the particular protein coats, or serovars, is not well settled, and what previously were thought to be various species of the genus Salmonella are now thought to be serovars of only two species by many researchers, S. enterica and S. bongori. However, these designations are not always accepted in the scientific literature and so common serovars that have been named in the past are still used (for example, S. typhi, S. typhimurium, S. enteritidis, S. cholerasuis, S. saintpaul). The serovars are identified by the Kauffman-White classification that uses two major types of antigens (somatic O and flagellar H) to distinguish the over 2,500 types of Salmonella bacteria. Sometimes laboratories or other reporting agencies identify isolates simply as Salmonella spp (species) and do not identify the serovars.
Autoimmune diseases are among the most heavily studied and poorest understood things I can think of.
As Mr. Pedantic said, there are mechanisms that eliminate self reactive lymphocytes during the maturation process. But these mechanisms aren't perfect. You can find self reactive lymphocytes in most individuals, but they are usually quiescent (anergic is the proper term).
In some cases, what seems to happen is that something triggers them out of their unreactive state. It might be a failure of the mechanism that supposed to suppress them (genetic or maybe something else), it might be a disease, or whatever.
There's an enormous amount of literature on autoimmunity, but very few clear answers, even in the case of what seem to be clear cut genetic problems.
A virus infection can incite the body to attack its own nerve tissue by activating unusual, disease-fighting cells with receptors for both viral and nerve proteins. The dual-receptor observation suggests a way brain and spinal cord nerve damage might be triggered in susceptible young adults afflicted with multiple sclerosis (MS).
University of Washington Department of Immunology scientists Qingyong "John" Ji, Antoine Perchellet, and Joan M. Goverman conducted the study, which was published June 6 in Nature Immunology.
This is thought to be the first study to reveal a mechanism for autoimmune disease that depends on destroyer immune cells expressing dual receptors for a normal protein made by the body and a pathogen.
Multiple sclerosis is one of many autoimmune disorders in which the body's lines of defense become misguided and start damaging normal tissue. In the case of multiple sclerosis, the protective sheath around major nerves -- the myelin -- in the brain and spinal cord disintegrates. Like a frayed electrical cord, the nerves no longer transmit a clear signal.
People with multiple sclerosis might lose their ability to see, walk, or use their arms, depending on which nerves are affected. The symptoms can appear, disappear, and re-appear. The disease is more common in women than in men.
In healthy people, the immune system is kept in check to tolerate the usual proteins and cells in the body, much like an eager watch dog is put on a leash and trained to ignore friends and neighbors, yet still protect the family.
"Autoimmunity is believed to arise from an accidental breakdown in this tolerance of the body's own proteins. This breakdown is triggered by something in the environment, most likely a pathogen," noted Goverman, professor and acting chair of immunology whose research concentrates on the origins of autoimmune disease. Her lab is studying mechanisms that maintain tolerance, as well as the "tripping" mechanisms that defeat it.
In their most recently published study, her research team genetically engineered mice that over-produce a certain type of white blood cell from a group known as killer T cells. The normal function of killer cells is to attack tumor cells or cells infected with viruses or other pathogens. These T cells have receptors that recognize specific proteins that infected cells display to them, much like holding up a target in a window.
The specific killer T cells examined in this study were CD8+ T cells. The Goverman lab engineered mice to over-produce CD8+cells that recognized myelin basic protein, a predominant protein in the myelin sheath that covers nerves. The major question investigated in the study was whether the genetically engineered mice would exhibit a disease that resembled multiple sclerosis.
The researchers infected the mice with a virus that has itself been engineered to produce myelin basic protein. This infection should activate the CD8+T cells to first attack the virally infected cells making myelin basic protein to eliminate the virus, then kill other cells that make myelin basic protein to wrap around nerves. Killing those cells would destroy the myelin sheath.
As expected, the mice developed a multiple sclerosis-like disease. But the researchers were surprised when viruses lacking the myelin basic protein also triggered the disease.
Additional cross-breeding experiments revealed the existence of two receptors on a few of the CD8+T cells. These cells, engineered specifically to bind to myelin basic protein, also built their own receptors for viruses, and could recognize both. When exposed to cells infected with viruses, they would bind to and destroy them using one receptor. Geared up as if they were beserk, some of these double-agent cells then would head elsewhere to bind their other receptor to cells producing myelin basic protein and ruin the coats on nerve cells.
"These results," the authors noted, "demonstrate a role for dual-receptor cells in autoimmunity." The study also points to why a ubiquitous viral infection could leave most people without any lasting effects, but trigger autoimmunity in genetically predisposed individuals.
The findings open a new perspective on the proposal that multiple sclerosis is virally induced, despite the inability to detect infectious virus in the central nervous system of multiple sclerosis patients. Data from other studies show that CD8+T cells can cross the blood-brain barrier, and also that multiple sclerosis patients have more central nervous system protein-specific CD8+T cells, compared to healthy people.
In the dual-receptor model, the autoimmune activity against nerve protein can continue after the virus is wiped out. Multiple sclerosis patients usually have high levels of antibodies indicating past infectious from several common viruses, but a live virus associated with multiple sclerosis has not been consistently observed. Therefore, to date, no specific virus has been confirmed as a causative agent for multiple sclerosis.
The authors explained that it's possible that multiple viruses could influence susceptibility to multiple sclerosis. The ability of any particular virus to contribute to the disease could depend on an individual's own repertoire of other predisposing genes, exposure to other predisposing environmental factors, and the random chance that T cells had been generated that recognize a myelin protein and a pathogen.
Receptors on T cells are randomly generated during their development. This observation helps explain why multiple sclerosis is partly a matter of chance. Some people with a genetic predisposition and environmental exposure develop the disease, while others with similar genetic predisposition and environmental exposure do not.
It's uncertain how common these dual-receptor T cells are, according to the researchers, although there are reports that up to one-third of human T cells express dual receptors. Goverman and her group plan to test samples from multiple sclerosis patients and see how many have dual-receptor T-cells.
A grant from the National Institutes of Health supported the study.
This study presents the first direct evidence for herpes simplex virus type 1 (HSV-1) infection in the neurons of the vestibular ganglion. Although many investigators have reported electron microscopic evidence of HSV-1 infection in sensory ganglia, HSV-1 infection in the vestibular ganglion has not been described. Vestibular ganglion neurons have a unique structure, with a loose myelin sheath instead of the satellite cell sheath that is seen in other ganglia. This loose myelin is slightly different from compact myelin which is known as too tight for HSV-1 to penetrate. The role of loose myelin in terms of HSV-1 infection is completely unknown. Therefore, in an attempt to evaluate the role of loose myelin in HSV-1 infection, we looked for HSV-1 particles, or any effects mediated by HSV-1, in the vestibular ganglion as compared with the geniculate ganglion. At the light microscopic level, some neurons with vacuolar changes were observed, mainly in the distal portion of the vestibular ganglion where the communicating branch from the geniculate ganglion enters. At the electron microscopic level, vacuoles, dilated rough endoplasmic reticulum and Golgi vesicles occupied by virus were observed in both ganglia neurons. In contrast, viral infections in Schwann and satellite cells were observed only in the geniculate ganglion, but not in the vestibular ganglion. These results suggest that loose myelin is an important barrier to HSV-1 infection, and it must play an important role in the prevention of viral spread from infected neurons to other cells.
During periods of multiple sclerosis activity, white blood cells (leukocytes) are drawn to regions of the white matter. These initiate and take part in what is known as the inflammatory response. The resulting inflammation is similar to what happens in your skin when you get a pimple.
During the inflammation, the myelin gets stripped from the axons in a process known as demyelination. The effect of this bears many parallels to the rubber insulation on wire perishing - some or all of the electricity in the wire will short out and the efficient conductivity of the wire will be reduced. When the myelin sheath is damaged, the transmission of nerve impulses is slowed, stopped or can jump across into other demyelinated axons.
Additionally, the inflammation can also damage the underlying axonal membrane. This membrane is a sophisticated structure that enables the nerve transmission (the action potential) to travel along the nerve.
It seems that the inflammation also kills the mainenance glial cells, in particular it seems to kill the myelin-producing oligodendrocytes, which are lost in great numbers. Almost no oligodendrocytes persist in the middle of chronic MS lesions.
At least, this has been the prevailing theory for the past few years. Now, however, several pieces of experimental work have produced results which challenge this model. Inflammation and oligodendrocyte loss are both found together in multiple sclerosis but which comes first? Does inflammation cause oligodendrocyte death, does oligodendrocyte death cause inflammation or are they both caused by a third process, perhaps a virus?
Recent research has looked at the brains of people who have died in the very early stages of MS lesion development and found that oligodendrocyte death actually precedes inflammation [Prineas et al, 2004]. It must be emphasised that these are the results of a very small study which have not yet been reproduced. Although few would deny that the inflammation contributes to MS damage, this work has the potential to turn the world of MS research upside-down. It suggests that looking for an autoimmune cause for MS may be misguided. It also challenges the current anti-inflammatory focus of most MS therapies. Are we, by analogy, treating a broken pipe by sticking a bucket under it rather than fixing the leak? That's not to say that these therapies don't produce results, just that tackling inflammation may not be the optimal stategy. For people with MS, this is a space to watch eagery.
Mice were inoculated with herpes simplex virus (HSV) type 1 by gently scraping the skin of the nose with a fine needle. About 80% of the animals developed latent inapparent HSV infections in trigeminal ganglia. Virus was demonstrable for at least 6 months post inoculation (p.i.) by cocultivation of ganglionic tissue with GMK cells. Histologically, trigeminal ganglia revealed infiltrations of inflammatory cells even 6 months p.i. In addition, lesions occurred in the brainstem corresponding to the entry of trigeminal roots, trigeminal tracts and nuclei. Inflammatory cell infiltration, disruption of myelin sheaths and macrophages laden with myelin degradation products were observed 7 days p.i. Fourteen to 30 days p.i. electron microscopy demonstrated completely naked axons. In the transitional region of the trigeminal root denuded axons occurred in the central part of the region while the peripheral myelin, bordering the demyelinated central segments, was intact. Small areas of demyelination were still detectable 3 and 6 months p.i. but there were then also signs of remyelination. Possible mechanisms causing the demyelination are discussed.