Herpes test score range definition,natural remedies for severe asthma,treatment for herpes eczema herpeticum - Plans On 2016

admin 07.05.2015

Natural killer cells are called ‘natural killers’ because they don’t need to be activated to kill cells that don’t have the right MHC markers on them. Recognizing the need for your average doctor to have access to a less expensive test of NK cell functionality, the CDC is working on one. They’re focusing on measuring how effective the receptors found on the surface of NK cells are at turning the cells on.
Because shipping has also been shown to reduce NK cell viability, they’re also proposing ways to optimize NK cell viability during the shipping process. A cornerstone of our immune defense, B-cells directly ‘attack’ pathogens and trigger other parts of the immune system to respond.
First, they are activated by antigens (proteins associated with pathogens) brought to them by macrophages and dendritic cells – two innate immune cells. Regulatory B-Cells – Cells regulating the powerful T-cell response (T-regulatory cells) received most of the attention until regulatory B-cells were discovered.
He noted that primary active infections – which occur when the body is first introduced to a pathogen – are often diagnosed via a high IgM response. Viral DNA with PCR isn’t effective either because it only tells us if the virus is present and it is present in 95-100% of population.
Viral mRNA using reverse transcriptase PCR, on the other hand, shows whether the virus replicating or not. Herpesviruses need to be able to attack and establish themselves in B-cells, ward off the immune system’s efforts to find them and then replicate when the time is right.
If there is evidence of genes associated with latency, but nothing is present, the virus is simply maintaining latent state. Because herpesvirus serology tests will not pick up this type of infection, however, it will never be picked up by standard serology tests. Learn more about EBV’s fascinating possible connection with autoimmunity in  Could the Epstein-Barr Virus – Autoimmunity Hypothesis Help Explain Chronic Fatigue Syndrome? Michael VanElzakker’s Vagus Nerve Infection Hypothesis (VNIH) for Chronic Fatigue Syndrome may be the most intriguing hypothesis to come along in the last twenty years. Apparently imaging techniques are not able yet to find localized infections in the vagus nerve. There’s interest because of this hypothesis, but most imaging of the vagus nerve thus far has been at the level of the brain, trying to understand the mechanism of vagus nerve stimulation for epilepsy or depression. You suggested that future CFS research  use radiolabeled antibodies to localize clusters of speci?c virus types. Another problem is that some of the pathogens that might be most likely to cause CFS are found in the vast majority of humans. Herpesviruses apparently love to set up house in the sensory ganglia, but you suggest that antiviral drugs might have trouble getting to them and destroying them there. Similarly to how the central nervous system has a blood-brain barrier (BBB), peripheral nervous system ganglia are immunoprivileged.
According to the vagus nerve infection hypothesis (VNIH), there is a physiological reason behind post-exertional malaise: Exercise provokes muscle tissue to produce the proinflammatory cytokine IL-6, which would then exacerbate the ongoing  local cytokine response within vagus nerve ganglia or paraganglia. In patients with HIV, reducing something like stress that taxes the immune system is bound to help a little bit. I understand that this is a really charged topic among CFS advocates, and there is a lot of misinformation out there. While CBT can help people with serious and chronic medical problems, it should be used as an adjunct and not a primary treatment. I should also say – CBT sometimes gets conflated with graded exercise therapy as well. Again, to be clear, if the VNIH is correct and some combination of glial inhibitor, antivirals and vagus nerve stimulation can be used to quell symptoms, then and only then does it make sense to begin graded exercise therapy. I absolutely do not condone forcing still-sick patients to exercise if it’s making their symptoms worse.
This has to do with the fact that the vagus nerve is a mixed cranial nerve, meaning it has both sensory (afferent, or towards the brain) and motor (efferent, or away from the brain) divisions. However, terms like over-active and under-active are a bit too simplified – what matters is that the nerve is able to respond and signal appropriately, to be able to create a functional signal-to-noise ratio.
Those of us who think that CFS is not psychologically-based tend to think there’s an immune dysfunction of some sort.
If a research group is unfamiliar with the cytokine literature they may have also made some easy mistakes in the cytokine assay – the actual lab methods for looking for these proteins. It wasn’t until recently that I discovered this unique journal, Medical Hypotheses, so I made some time to write up the idea. The week the paper came out, Anthony Komaroff contacted me, we’ve been in contact since. I also know that the paper is already being taught at some universities and medical schools, so hopefully it will at least get young scientists to start thinking about CFS. Even if the hypothesis doesn’t turn out to be accurate, or is only partially accurate, I hope that it gets us closer to effective treatments that are actually attacking the root causes of CFS symptoms and not just helping people cope with them. It’s the Vagus Nerve Infection Hypothesis (VNIH) for chronic fatigue syndrome, and it could change how this disorder is viewed, researched and treated. Created by Michael VanElzakker, a Tufts neuroscientist,  the VNIH proposes that nerve loving viruses trigger a difficult to detect  immune response which produces the fatigue and other symptoms present in chronic fatigue syndrome. Most humans carry several of these herpesviruses in latent form unless some stressor or biological event allows them to become reactivated. VanElzakker believes that upon reactivation these viruses replicate and move outside the nerves where they run into glial cells that attempt to gobble them up. Receptors on the vagus nerve that sniff out these alarm signals tell the brain an infection is present, which then shuts the body down by sending out  signals  (fatigue, flu-like symptoms, pain, etc.) that slow the body down, tell it to stop moving, stop eating, stop thinking. Because these infections are localized right on the main immune conduit to the brain, VanElzakker believes they don’t need to produce the outsized cytokine response researchers have been looking for. Glial cell  release of cytokines, glutamate, free radicals, etc.  in the dorsal horn of the spinal cord causes  increased pain sensitivity and allodynia in susceptible individuals.
There is no  reason to suspect  that vagus-nerve associated glia would function any different than pain associated glia.
Nobody knows what a herpesvirus infection  of the vagus nerve would look like,  but VanElzakker doesn’t see any  reason it should look any different  from an infection in other parts of the body.
We know a  herpesvirus infection of your trigeminal nerve gets you shingles and chronic pain.  Researchers believe a chronic infection in the dorsal horn of your spinal cord will can  get you fibromyalgia and allodynia.  Would  an  infection of the vagus nerve get you sickness behavior and  chronic fatigue syndrome? What if the vagus nerve receptors were…ceaselessly bombarded with these cytokines?  The symptoms of sickness behavior would be severe and intractable. They found that the glial cells  reared up and starting producing pro-inflammatory cytokines to take care of the intruder. VanElzakker suggests animal studies to better understand infections of the vagus nerve and to ultimately to build a chronic fatigue syndrome rodent model would be helpful.  Magnetic resonance imaging (MRI) may be able to detect viral lesions in central nervous system tissues. If VE’s theory is correct then glial cell inhibitors to stop the immune activation, antivirals to attack the pathogens, vagus nerve stimulation and surgical alteration of the vagus nerve might be possible treatments sometime in the future. Glial cell inhibitors have a good safety profile, have been helpful at curbing neuropathic pain and are not used much in chronic fatigue syndrome or fibromyalgia. If VanElzakker is right then Ibudilast, a drug in clinical trials now for another disorder, is a possibility. Ibudilast is also  known to have neuroprotective and vasodilative effects and is usually used to treat asthma and stroke.
The NIH is funding Ibudilast trials in the US to see if it’s effective against drug addiction.
Other general microglial inhibitors exist (minocyline, pentoxyfilline, propentfylline) but have undesirable side effects. Stopping glial cell activation may be easier than getting at the viruses themselves.  Herpesviruses living in the sensory ganglia may be protected from antiviral drugs and antibodies. VanElzakker also notes that while behavioral therapies are not curative and may only apply to a subset of patients, they can help moderate symptoms and improve quality of life in some. The VNIT may be able to explain more puzzling aspects of chronic fatigue syndrome than any other. The pathways researchers and doctors take to get to disorders like FM or chronic fatigue syndrome are nothing but diverse, and it’s worth taking a look at how Dr. Pridgen saw a pattern emerge in his  treatment of thousands of patients with chronic gastrointestinal issues that intrigued him. Shorter and shorter relapses over time in his patients lead Pridgen to conclude that a virus must be involved.
The problem, he thought, had to be some sort of pathogen that was steadily increasing with every recurrence. HSV-1 has been found in the esophagus, stomach and duodenum of the gastrointestinal system. Pridgen’s patent application indicates that he believes that stressors and  peptides and hormones released by the sympathetic nervous system and HPA axis  set the stage for herpes simplex-1 reactivation. Once  these neurons and ganglia are damaged, Pridgen believes they send out signals that ultimately muck up the pain processing centers in the central nervous system.
One of Pridgen’s patent applications suggests that one of his unique insights has been to combine valacyclovir (valtrex) with an anti-inflammatory, Celecoxib (Celebrex) that has antiviral properties.
Celexcoxib (Celebrex) is a non-steroidal antinflammatory (NSAID) COX-2 inhibitor usually used  in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms. Pridgen and Duffy are looking for herpes simplex virus, but other herpes viruses could be affected by this treatment. They are also the only immune cells that can recognize infected cells without antibodies and MHC markers being present. This involves keeping cells in their natural habitat – the whole blood – and isolating PMBC’s first. Knox echoed Mady Hornig’s statements that there are “lots of vacuums in this field” and then went onto a short overview.
B-cells then produce hordes of pathogen specific antibodies that search for the pathogen outside the cell and attach to it in order to prevent it from attacking our cells. These antibodies are derived from unusual sugar residues synthesized in the gut – an interesting finding given the emphasis both Dr.
Regulatory B-cells make up only 0.5% of total B-cells but are powerful regulators of immune activation and inflammation. Once activated, though, in people with poorly functioning immune systems such as transplant patients, these seemingly innocuous viruses can cause enormous damage. They are complex viruses with big genomes that have genes associated with maintaining latency, with altering the immune response and with building new viruses. If genes produced later in its life cycle are found, the virus is active but not replicating. Lerner and researchers at Ohio State University proposes EBV is perturbing immune cells and causing immune cell dysfunction without causing cell death, while producing only very low levels of viral transcription. I mostly focus on posttraumatic stress disorder (PTSD), which I consider to be very different from CFS and a separate arm of my research interests (although there are many interesting overlaps between the views of CFS and PTSD within our culture). Some of the many research programs there related to neuropathic pain, cytokines, and the vagus nerve.
It’s difficult to convince funding agencies to give us money to pilot test a method so that we can even begin to ask questions about a hypothesis that may or may not be accurate. I laid out a protocol in the paper for creating an animal model; I hope somebody with a rat lab takes the idea and runs with it. So, radiolableled antibodies against HHV-1 would find a signal in most people, but only cause CFS if the viruses are in a vagus (para)ganglion.
According to the hypothesis, the frequent failure of drug therapy and also one’s own immune system to eliminate infections within vagal ganglia and paraganglia is just like how some drug doses and antibodies do not penetrate the BBB. So, if someone who doesn’t like public speaking is giving a presentation, their immune system is generating a cytokine response.
Just to be clear, cognitive-behavioral therapy (CBT) does not get at the root cause of CFS. It would be crazy, for example, for a doctor to prescribe CBT instead of chemotherapy for cancer. At that point, the root cause of CFS symptoms has been dealt with, and the next priority is to deal with muscle deconditioning which is not an insignificant factor in ongoing symptoms. Its parasympathetic influence over the body results from efferent activity; its function in detecting peripheral infection and triggering sickness behavior results from afferent activity.
People have been looking for cytokines because they are an obvious potential link between the immune system and CFS symptoms, but a lot of studies have ignored how cytokines work.
If someone who didn’t know any better stored their blood samples in a refrigerator instead of a -80° freezer, you can bet they did not find cytokines. I’ve had the idea for quite a long time, and spent a lot of time and effort trying to set up a collaboration with a rat lab, to create an animal model.
It gave me a forum to really give people the background they needed to understand the idea, and allows people to check the citations themselves.
I hope people start to think about new CFS findings through the lens of this hypothesis because in my experience, it explains a lot of phenomenology. At some point the constant production of these excitatory substances  causes  a switch to get flipped sending the pain response spiraling upwards instead of shutting down. VanElzakker proposes the same process  causing pain sensitization in the dorsal horn is  causing fatigue and other symptoms in chronic fatigue syndrome, except this time it’s associated with glial cells surrounding the vagus nerve.
Lerner’s theory), could trigger the similar type of hypersensitive reaction in the vagus nerve. If it’s infected in your  abdominal area, you might find cytokines in the blood, but it might be hard to find them in your spinal fluid.
It is not yet known if  PET scans can detect the activation of a different type of glial cells; the satellite glia that are in vagus nerve ganglia and paraganglia, but special PET scans might be able to be used to assess microglial activation. The over-generation of neurotransmitters such as glutamate, Substance P, serotonin, norepinephrine, dopamine, brain-derived neurotrophic factor (BDNF) involved in this process then causes central sensitization. Pummeling the virus with that one-two punch, he believes, will finally stop the virus from reactivating. Immunologists were invited to give presentations and then queried regarding whether immune tests should be incorporated into diagnostic protocols for this disorder.  Dr. They propose a pilot study to determine ways to optimize viability of NK cells during shipping.
They also take that antigen and present it to killer T-cell’s which then mount a pathogen specific defense which gets at pathogens located inside the cell. They induce two important anti-inflammatory cytokines (IL-10, TGF-beta), which dampen the inflammation produced by the innate immune system. With their immune systems intentionally knee-capped in order to avoid an immune attack on their transplanted organ, they are ripe for herpesvirus activation. If genes devoted to building the outer membrane of the herpesvirus are present – you have an active, replicating virus on your hands. All it took was for someone who was thinking about CFS to be exposed to these different literatures and to start fitting them together. I’m not jealously guarding these ideas, I put them in the paper in the hopes that other groups would work on them too. Is it possible to radiolabel antibodies so that they pick up clusters of infection in the body? One is that antibodies are specific, but CFS could be caused by a number of different pathogens. If such a person even thinks about giving a presentation, they are likely to generate a cytokine response. I have hypothesized that CFS is a neurological illness triggered by a foreign pathogen infecting the vagus nerve.
In the paper I gave an example of a treatment regimen that included graded exercise therapy. When they do find them sometimes research groups find similar cytokines and sometimes they don’t. If blood samples went through freeze-thaw cycles, the cytokines will also start to denature (break down). Cytokine responses are very complex, they interact with each other and they change in daily and hourly rhythms. Based on past experience, I thought I’d have to keep cold-calling researchers to push the hypothesis.
I’ve been in contact with a lot of other well-known CFS researchers, and I think the idea is at least changing the way that some people think about the problem.
There are a lot of technical issues but we’re hoping to use functional imaging to gain enough preliminary data that we can pursue it further. If your vagus nerve is infected near your brainstem you might find cytokines  in the spinal fluid, but you probably won’t find them in your blood. Then he found that adding an anti-inflammatory (which also had anti-viral properties) reduced their fatigue, gastrointestinal complaints, depression and anxiety markedly and improved their energy.
So, we could flood someone’s body with radiolabeled antibodies against HHV-6, but maybe in that specific case, their symptoms are caused by HHV-4 (Epstein–Barr). Another problem is that antibodies cannot always get inside ganglia, which are immunoprivileged. The three out of ten that found some slight improvement may have used CBT to figure out exactly what level of activity they should be worried about.
Cytokine studies are quite prone to false negatives, and it’s a mistake to infer from a negative cytokine blood test that there is no cytokine response happening anywhere in the body. There are definitely a lot of really good researchers who have looked into cytokines, but the literature can get muddied pretty easily by bad studies. But despite all of that, I still think it’s a research program that is worth pursuing. So, the moderate improvements they reported in a minority of patients were probably related to stress reduction. CBT for CFS patients can reduce stress, which is one mechanism of action to improve symptoms.
You mentioned that lung infections are also not associated with increased cytokine levels in the blood.  Are there many other infections like this? If you’re seeing a CBT practitioner who views CFS as a psychologically-based illness and is approaching your CBT that way, fire them.



Side effects of taking herpes medication
Time and energy management tips
  • BEZPRIDEL, 07.05.2015 at 17:36:35
    Since I switched to a greengrocer for all my fruit and veg two and discomfort that was.
  • miss_x, 07.05.2015 at 20:56:35
    Controlling both the virus' shedding and the eye.