Soms in combinatie met erfelijke aanleg.
Het immuunsysteem blijft na een virusinfectie cellen in het eigen lichaam aanvallen omdat de eigen eiwitten lijken op de eiwitten die het immuunsysteem moest aanvallen door de infectie. Het valt bijvoorbeeld de Intrinsic factor aan (r-factor) noodzakelijk voor de opname van vele B vitamines. In de mitochondrien zitten overeenkomstige eiwitten die ook worden aangevallen waardoor de mitochondrien minder goed werken.
Intrinsic factor is a protein made by the stomach that helps the body take in B1\ \
het virus geelimineerd is zijn
de antilichamen nog steeds
aanwezig. Omdat deze
antilichamen nog steeds de
eiwitten zien, blijft het actief.
steeds met een virus te maken te
Er wordt ook steeds aan getwijfelt of het onderdrukken van een virus zinvol is.
Er wordt vaak gedacht aan een behandeling die de werking van het immuunsysteem afremt.
Het virus kan maar hoeft niet meer aanwezig te zijn. Maar een virus (met mogelijk een vergelijkbare uitwerking) moet wel eerder aanwezig zijn geweest.
CVS wordt veel gezien na een ziekte. En CVS blijft dan bestaan.
Er is ook
een sterke verdenking naar het
niet goed functioneren van het
De mitochondrien werken niet goed bij CVS.
Antistoffen tegen intrinsic factor zijn specifiek voor pernicieuze anemie en worden niet aangetroffen in de algemene bevolking. Er bestaan twee soorten intrinsic factor antistoffen: antistoffen die competeren met de binding van vitamine B12 aan intrinsic factor in de maag (50% van de patiŽnten) en antistoffen die de opname van het vitamine B12-intrinsic factor complex in het terminale ileum blokkeren (35% van de patiŽnten).
De meest gangbare bepalingen hebben de hoogste gevoeligheid voor het eerste type antistoffen. Antistoffen tegen intrinsic factor zijn zeer specifiek voor pernicieuze anemie. Aangezien antistoffen tegen intrinsic factor slechts bij 50-70% van de patiŽnten met pernicieuze anemie worden aangetroffen, dient bij blijvende klinische verdenking altijd aanvullend een bepaling voor antistoffen tegen pariŽtale cellen te worden uitgevoerd.
Bij coeliakiepatiŽnten (auto-immuunziekte van de darm) en dan wel voornamelijk bij hen die geen glutenvrij dieet gebruiken, zijn vaak antistoffen (met name IgA) tegen reticuline, endomysium, tissue-transglutaminase (tTG) en gliadine aantoonbaar.
Voor al deze antistoffen geldt, dat er een relatie is met de mate van vlokatrofie; de antistoffen verdwijnen als de patiŽnten een glutenvrij dieet gebruiken, en bij de meeste patiŽnten worden de antistoffen weer aantoonbaar bij glutengebruik. Coeliakie kan een tekort aan vitamine B12 veroorzaken. De opname van vitamine B12 kan verbeteren en zelfs herstellen indien het glutenvrij dieet gevolgd wordt, en het darmslijmvlies herstelt.
overwhelming majority (roughly
90%) of chronic diseases are not
inherited, but result from
environmental damage to cellular
DNA or cellular processes.
A person's sex also seems to have some role in the development of autoimmunity, classifying most autoimmune diseases as sex-related diseases. Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women.
Viral infections in humans commonly result in the transient appearance of a variety of autoantibodies and, in some patients, the development of autoimmune tissue injury and disease. The capacity to cause or exacerbate an autoimmune process is common to many viruses, affecting mainly organs injured by the replicating virus, as demonstrated by several animal models. Viral "footprints" can often be found in patients with autoimmune diseases and include high titers of specific antiviral antibodies, identification of viral (retroviral) sequences, and the presence of alpha-interferons in the serum. Several mechanisms that are not mutually exclusive can account for the pathogenesis of virus-induced autoimmunity. Viruses may modify or release sequestered cellular proteins or affect the host's immune system by direct polyclonal activation of B cells, effects on immunoregulatory cells, and release of lymphokines. The appearance of antiviral antibodies may also be deleterious to the host through molecular mimicry, the generation of anti-idiotypic antibodies, or the formation of immune complexes. No single microorganism or mechanism can explain the extremely varied phenomena of autoimmunity, but growing evidence suggests that certain viral infections may lead to clinically manifest autoimmunity in individuals having genetic and possibly other predisposing factors.
Pernicious anemia is an autoimmune disorder characterized by atrophy of the gastric mucosa, selective loss of parietal and chief cells from the gastric mucosa, and an infiltration of lymphocytes into the submucosa. Immunologically, pernicious anemia is characterized by autoantibodies to gastric parietal cells (AGPA), proton pump (H+K+ATPase), and to the cobalamin-absorbing protein, intrinsic factor. Intrinsic factor is a 60 kD glycoprotein produced by the parietal cells of the stomach lining that enables the absorption of vitamin B12. Two types of intrinsic factor antibodies can occur. Type I antibodies block the binding of vitamin B12 to intrinsic factor, thereby preventing the uptake of vitamin V12. Type II intrinsic factor antibodies bind to intrinsic factor and prevent the attachment of intrinsic factor-cobalamin complex to receptors in the ileum. Both types of antibodies prevent absorption of cobalamin.
Autoimmune gastritis is also called type 1 chronic gastritis. Chronic gastritis type 2 is a similar disease caused by Helicobacter pylori infection. Over type patients with chronic H pylori infection can develop autoimmune gastritis. In autoimmune gastritis, the mucosal cells of the intestines are destroyed by autoantibodies to gastric parietal cells. Unlike pernicious anemia, autoantibodies to intrinsic factor are not presenting autoimmune gastritis. However, chronic autoimmune gastritis may progress to pernicious anemia. This process may take 20 to 30 years, which suggests that autoimmune gastritis is an early phase of pernicious anemia.
AGPA antibodies occur in about 90 percent of patents with pernicious anemia, 30 percent of first-degree relatives of patents with pernicious anemia, and they are also seen in up to 50 percent of adults and 18 percent of children with Helicobacter pylori infection. In addition, AGPA antibodies are seen in patients with various autoimmune endocrinopathies, including autoimmune thyroid disease. 2-8 percent of normal elderly subjects may also have AGPA antibodies, and the incidence of atrophic gastritis increases with age.
An interesting inverse relationship exists between infectious diseases and autoimmune diseases. In areas where multiple infectious diseases are endemic, autoimmune diseases are quite rarely seen. The reverse, to some extent, seems to hold true. The hygiene hypothesis attributes these correlations to the immune manipulating strategies of pathogens. Whilst such an observation has been variously termed as spurious and ineffective, according to some studies, parasite infection is associated with reduced activity of autoimmune disease
Enzym Gepotentieerde Desensibilisatie zou misschien gebruikt kunnen worden om het immuunsysteem te leren niet meer die eiwitten aan te vallen. Maar alleen als het virus er niet meer is. Als het virus er nog is dan is het het beste om er een zo goed functionerend als mogelijk immuunsysteem tegen te hebben en om een antiviraal middel te hebben alwaar nu veel onderzoek naar gedaan wordt. Raltegravir en XMRV
De aanval van het immuunsysteem
op de eiwitten in de
mitochodrien verklaart mogelijk
Door het virus blijft het immuunsysteem chronisch actief. Dan ben je constant ziek.
Just to explain the significance of this. The XMRV virus contains proteins that are very similar to the proteins expressed in human mitochondria, the powerhouses of the cell, responsible for respiration and energy generation. They are also similar to proteins involved in prostate cancer. These viral proteins are antigenic, and antibodies to the virus may also target their human counterparts and interfere with their function.
Even if the immune response has successfully eliminated the virus, the antibodies are still present, and because they keep on meeting the human lookalike proteins, the immune response becomes self-sustaining. This may explain the controversy regarding the presence or absence of the virus. The XMRV virus doesnít have to be there, it just needs to have been there at some time in the past. The more effective the immune attack on the virus, the greater the danger of autoimmunity.
Based on a series of studies in mice, they said cytomegalovirus or CMV -- a herpes virus that affects some 60 to 99 percent of adults globally -- appears to increase inflammation in blood vessels, causing high blood pressure.
And when combined with a fatty diet, CMV may also cause hardening of the arteries, a major risk factor for heart attacks, strokes, and kidney disease, they said.
"I think it could be very important," said Dr. Clyde Crumpacker of Harvard Medical School and Beth Israel Deaconess Medical Center in Boston, who worked on the study in the Public Library of Science Journal PLoS Pathogens.
"It may suggest a whole new way of looking at high blood pressure and vascular disease," Crumpacker said in a telephone interview.
He said the research offers the first direct proof that the virus causes persistent infection in blood vessels. Doctors typically use generic drugs such as beta blockers and ACE inhibitors to control blood pressure, a condition that affects one in every three adults in the United States.
Crumpacker said the study suggests vaccines and antiviral drugs may offer a new approach at treating hypertension.
Currently, there is no vaccine, but several companies, including Sanofi-Aventis, Novartis , GlaxoSmithKline PLC and Vical, are working on them.
And Swiss drugmaker Roche Holding AG makes an antiviral drug called Valcyte to prevent CMV infections in transplant recipients.
CMV AND DIET
By age 40, most adults will have been exposed to CMV, although many never experience any symptoms. But the virus can cause harm in people with compromised immune systems, such as transplant recipients, and it is a major cause of birth defects in babies whose mothers were infected during pregnancy.
In one experiment, Crumpacker and colleagues examined four groups of lab mice. Two were fed a standard diet and two were fed a high fat diet. After for weeks, half of the mice from the standard and fatty diet groups were exposed to the virus.
Six weeks later, mice in both infected groups had elevated blood pressure, but 30 percent of infected mice on high cholesterol diet also showed signs of atherosclerosis.
"This strongly suggests that the CMV infection and the high cholesterol diet might be working together," Crumpacker said.
In another study of kidney cells in infected mice, the team found high levels of the enzyme renin, which is known to cause high blood pressure. They found the same high rates of the enzyme in human blood vessel cells infected with CMV.
And they found that CMV infection increased markers for inflammation in blood vessels.
More research is needed looking at the role of viruses in causing heart disease, but Crumpacker said the findings suggest new treatment possibilities.
"Some cases of
hypertension might be treated or
prevented by antiviral therapy or a
vaccine against CMV," he said.
Common Virus May Cause Asthma
Any infection caused by a virus can cause major complications for an asthmatic. In fact, many asthma experts, including those at the Mayo Clinic, believe viruses "are the most common cause of asthma flare-ups, especially in children.
Another common virus is the Respiratory Syncytial Virus (RSV). This little pest is known to cause a common head cold in adults, yet in children it can cause bronchiolitis, and RSV pneumonia, which can lead to asthma trouble and even respiratory failure.
Do Viruses Cause Asthma?
As noted by the Food and Drug Administratino (FDA) in this post, new research shows that not only do viruses trigger asthma, they may also cause some children to develop asthma. Since RSV is a common virus, and most infants are exposed to it early in life, it's believed to be the most common virus to cause asthma.
Likewise, studies show that children who develop RSV pneumonia are at an even greater risk for developing asthma.
To understand how viruses cause asthma, we must first revisit the Hygiene hypothesis, which is basically an "educated guess" that postulates that one develops asthma during the first three months of life when the immune system is maturing.
The basis of this hypothesis is that in our modern society children are not being exposed to enough bacteria, and therefore aren't being exposed to enough bacterial lipopolysaccharide (LPS). In other words, we are too clean.
LPS is a molecule on bacteria that, according to the FDA, "stimulates and educates the immune system by triggering signals through a molecular 'switch' called TLR4, which is found on certain immune system cells."
Thus, when the level of LPS is low in the environment around the child (not enough bacteria), the immune system does not develop properly.
The immune system therefore becomes bored and creates a defense against things that normally don't pose a threat to their bodies, such as dust mites, cockroach urine, pollen, grass, molds, fungus and other allergens
U.S. researchers explain why flu virus more active in winter
SUNDAY MARCH 2, 2008 (Foodconsumer.org) -- It's a fact that influenza viruses and probably some others are more active in the winter. U.S. researchers released a report Sunday saying that it is the fatty material put on the flu viruses that hardens and protects them at colder temperatures.
Joshua Zimmerberg of the U.S. National Institute of Child Health and Human Development (NICHD) and colleagues found only when the butter-like coating melts in the respiratory tract could the flu virus invade cells.
It's commonly believed that the reason why it's easier for people to get flu in the winter time is because they stay indoors longer and the flu virus is less likely to get killed by the sun. But Zimmerberg and team suggested that explanation is insufficient.
The finding reported in the journal Nature Chemical Biology would provide a target for researchers to find new ways to prevent and treat flu, NICHD Director Duane Alexander was cited by Reuters as saying.
Flu viruses cause a mild illness and do not cause too much harm without medical intervention in many cases, but those with immune systems compromised are at a higher risk of complications.
The U.S. government says that 36,000 people in the United States die from flu implications each year. But some source suggests that the real number of death from flu viruses is about 1 to 1.5 % of these 36,000 people, meaning that the mortality is rare.
There are a few things people may do to help prevent the winter flu:
1) Avoid sugar: It's believed that too much sugar could hamper immune response and lower your capability of defending against the winter flu;
2) Avoid stress and get enough rest: Stress and fatigue sabotage your immune system;
3) Eat garlic regularly: Garlic kills flu viruses in addition to bacteria and fungi;
4) Exercise: Exercising can get your needy nutrient to its right position quickly to help your immune system to defend against the winter flu viruses;
5) Keep windows slightly always: In the winter, windows are often tightly closed to save energy. But many people do not realize this could increase the chance for you to spread or to get flu viruses;
6) Wash your hands: Dirty hands can spread germs and flu viruses easily.