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\ \
Ook nadat
het virus geelimineerd is zijn
de antilichamen nog steeds
aanwezig. Omdat deze
antilichamen nog steeds de
menselijke overeenkomstige
eiwitten zien, blijft het actief.
CVS lijkt
steeds met een virus te maken te
hebben.
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
immuunsysteem.
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 patiënten) en antistoffen die de opname van het vitamine B12-intrinsic factor complex in het terminale ileum blokkeren (35% van de patiënten).
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 patiënten met pernicieuze anemie worden aangetroffen, dient bij blijvende klinische verdenking altijd aanvullend een bepaling voor antistoffen tegen pariëtale cellen te worden uitgevoerd.
Bij coeliakiepatiënten (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 patiënten een glutenvrij dieet gebruiken, en bij de meeste patiënten 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.
The
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.
overzicht autoimmuunziektes
Pernicious Anemia
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
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.
inverse relationship
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
de vermoeidheid.
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 doesn’t 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.