Biologisch Medisch Centrum |  Chronisch Vermoeidheids Syndroom | Paul van Meerendonk Utrecht Epe
Virus en Autoimuunziekte


 

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Een combinatie van Virussen veroorzaakt Autoimuunziekte
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\ \B2\ \B6\ \pantothenic acid\ \folic acid\ \niacin\ \biotin\  vitamin B12.
 

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.
 

Een tekort aan vitamine B12 ontstaat ook als iemand geen intrinsic factor (een glycoproteÔne) maakt. Dit is bijvoorbeeld het geval na een operatieve verwijdering van een deel van de maag. Ook kan het voorkomen dat het lichaam antistoffen tegen deze factor maakt, waardoor de opname door het lichaam wordt geremd.

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.


 
Pernicious anaemia is an autoimmune disease. An autoimmune disease is a condition caused by antibodies from your immune system attacking your body. Your immune system mistakes your own tissue as foreign and attacks it, causing inflammation. If you have pernicious anaemia, the inflammation happens in the lining of your stomach.

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 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.
 

 




 


 


 

Dr Chia on viruses, cfs and Oxymatrine

We have noticed that patients often would have two symptomatic infections before developing ME/CFS; the two episodes could be occurring within one year or years apart. In animal models, one can demonstrate that a prior viral infection can predispose to more severe, subsequent enterovirus infection. I believe, although this is difficult to prove in humans, that pre-existing antibody against a prior strain of virus can bind to, and yet not able to neutralize, the new viruses, and eventually result in uptake by the monocytes. These infected monocytes become the "Trojan horses" that would home into the tissues such as brain, heart and muscles (tropism) and become macrophages. This process could be associated with variable inflammatory symptoms. One could not even start to suspect the "Trojan horses", if the process is clinically silent !

(Dr. Chia appears to be elucidating the following process; an enteroviral attack results in the production of antibodies against that one strain of enterovirus. Upon a subsequent second attack by a slightly different strain, the immune system misfires and - instead of creating new, different antibodies - , raises the same antibodies, which bind to but are not able to completely neutralize the new virus. Immune cells called monocytes pick up these incompletely neutralized viruses and themselves get infected. As they travel around the body they infect other tissues.)

A closely spaced infection may predispose to a more severe, second infection when the immune response has not shifted back to normal. A shift to the Th2-dominant response occurred when patients received steroids at the onset of the respiratory illness associated with asthma, or when they developed "allergic rashes" after eating shellfish, or severe neck or back pain. Many of the patients who developed recurrent respiratory infections, often with asthma or allergic rhinitis, during childhood are Th2 -polarized in response to the next infection. If the infective pathogens do not persist in the body, then nothing more will happen. If the next infection is capable of persisting in the body, such as EBV, enterovirus, adenovirus, parvovirus and others, then chronic infection will occur.

An appropriate immune response, manifested as fevers, nausea, vomiting along with flu-like symptoms in acute hepatitis B, would usually eradicate the viral infection. But minimal inflammatory symptoms at the onset of this type of infection is often followed by chronic persistence of hepatitis B infection. An appropriate immune response is paramount in controlling and eradicating the initial infection.

(Again this suggests that an inappropriate immune response in ME/CFS patients does not eradicate the virus. This theory contrasts with findings of the Dubbo project which suggest that ME/CFS patients tend to have more severe symptoms during the triggering infection and a heightened cytokine response compared to people with the same infections who did not come down with the disease.)

There is no doubt that an inappropriate immmune response to persisting pathogens is an integral part of this illness, as in tuberculosis or any other disseminated infections.

If I understood this correctly, when you put biopsy tissues into culture the viruses didn't grow out unless you blocked the immune response. Does this mean that viral infections in chronic fatigue syndrome (ME/CFS) patients persist at least in part because of a problem with the immune response?

This was the only way we could grow viruses from human stomach tissues in monkey kidney cells. The in vitro finding does not necessarily correlate with the in vivo situation, but "this thinking" led to the experimental conditions that allowed us to grow the non-cytopathic virus. There is no doubt that an inappropriate immmune response to persisting pathogens is an integral part of this illness, as in tuberculosis or any other disseminated infections.

Do you accept gut biopsies from patients for testing for enteroviruses? If so, how do they arrange to have them sent to your office? What is the cost? Should they send more than one if possible?

The best area to biopsy is the antrum of the stomach, which is also the best place to look for H. pylori. We will need 5 unstained slides, on charged slides for immunochemical staining. The charge is $250 for the staining. This test is far more sensitive and specific as compared to serum antibody and serum viral RNA testing. The results of the comparison will be presented at the next IACFS meeting. See the attached test request form for more details.

Dig Deeper! For a test requisition form to have Dr. Chia analyze whether pathogens are present in stomach biopsies gathered during an endoscopy.

Treatment

Is there an effective treatment for these viruses? Are strong anti-virals needed? Will immune supportive therapies help? How about therapies designed to aid the gut such as probiotics?

What is the ultimate drug useful for the chronic viral infection remains unclear. I believe that antivirals directed against RNA replication (interferons) will be useful for this illness. Immune support or modulation may help but these viruses are capable of controlling our immune responses to allow their own persistence. Probiotics may help to change the microbial flora but will not change the viral infection in the lining of the gut.

Dig Deeper! Interferon's and Chronic Fatigue Syndrome (ME/CFS) Treatment

Itís been reported that some antivirals temporarily worked quite well but that your patients tended to relapse after the therapy has been stopped. This is an atypical response to anti-virals is it not? Whatís going on here?

The good news about what we have shown in our patients is that CFS is a treatable disease even if they relapsed after treatment.

It is not an atypical response if one assumes the infection is chronic and persistent. Do any antivirals for HIV actually cure the disease? One would be totally surprised if HIV does not rebound (relapse) when one stops HAART (highly active anti-retroviral therapy) in these patients, and the same often apply to hepatitis B and C. Do antiviral drugs cure herpes virus (HSV1 or 2)? Recurrence of disease is common after treatment for cold sores or genital herpes but this does not make the antiviral an ineffective treatment for the disease. The good news about what we have shown in our patients is that CFS is a treatable disease even if they relapsed after treatment. With better and more tolerable treatment, we should be able to control the symptoms and even put the patient into remission, but a cure may be difficult to achieve.

As someone whoís treated over a thousand chronic fatigue syndrome patients could you outline what youíve found to be more effective in treating the following symptoms:

My approach is not different from anybody else when treating the symptoms.

  • Poor sleep: any medications for sleep but the usual hypnotics do not work well. Most of the patients need more powerful drugs.
  • Fatigue: stimulants such as Ritalin or Provigil. The effect is quite variable.
  • Pain: Ultram or ultracet. Fetanyl patch seems to work better than the higher potency narcotics.
  • Problems with concentration: stimulants as above.
  • Depression/anxiety: SSRIs and anxiolytics.
  • Orthostatic intolerance: Midodrine

Dig Deeper! Midrodrine and Chronic Fatigue Syndrome (ME/CFS) Treatment

Dig Deeper! Ritalin and Chronic Fatigue Syndrome (ME/CFS) Treatment

Dig Deeper! Pharmaceutical Drugs For Sleep in Chronic Fatigue Syndrome (ME/CFS)

Weíd like to get more funding to study Chinese herbs, since "Western medicine" is not going to come through for many years, especially when people are studying different viruses after 28 years of investigation

Several of your patients have mentioned that youíre trying oxymatrine. Is it an important part of your protocol? Are there any other over the counter immune enhancers you recommend or are exploring?

We have tried a number of Chinese herbs alone or in combination. The response is variable. Oxymatrine could boost the immune response, and we will present data at the next IACFS meeting. Weíd like to get more funding to study Chinese herbs, since "Western medicine" is not going to come through for many years, especially when people are studying different viruses after 28 years of investigations. Some of the OTC (over the counter) immune enhancers have not been too helpful when tested in a carefully controlled study conducted by the National Institute of Complementary and Alternative Medicine. Thymosins from other species are not effective in the human since these proteins are species-specific.

(After a talk with Dr. Chia's son, Andrew, a patient of Dr. Chia's reported that Andrew received substantial benefit from Chinese herbs. The interferon course helped greatly but he was still plagued with a sore throat and could not exercise consistently. The Chinese herbs put him over the top and he is healthy today. She reported that about 50% of ME/CFS patients receive substantial help from Chinese herbs)

Dig Deeper! Oxymatrine and ME/CFS

The Future

Your attempts to identify the specific viruses (varicella-zoster, parainfluenza viruses, adenovirus and respiratory syncytial virus) present probably failed, as you noted, because of some technical problems. Is it necessary to identify the specific enteroviral agent present in order to come up with the right therapy? Where do you go now in your attempts to identify the pathogens?

The failure to identify these agents by staining did not mean the testing failed but rather meant these viruses were not found in stomach by our testing. We have used multiple antiviral antibodies to see if other agents are in the stomach. The absence of other viral agents made the enterovirus even more important in our paper.

The NIH turned its back on pathogen research in chronic fatigue syndrome (ME/CFS) a couple of years ago. You, Dr. Montoya and Dr. Lerner, however, have recently come out with studies suggesting pathogens can play an important role for at least some chronic fatigue syndrome (ME/CFS) patients. You attended the Grantsmanship Workshop held by the Office of Research for Womenís Health (ORWH) last September that was designed to provide CFS researchers opportunities outside of the NIHís CFS research program. How did that go for you? Did you find any funding opportunities?

I appreciated the opportunity to go to the Grantsmanship Workshop and met the delightful directors/leaders of ORWH who are genuinely interested in helping with this elusive illness. There are funding opportunities for CFS but there is not yet a clearly designated source of funding where one can easily get money. The funding will probably take 24 months from the start of the grant writing process, approval process and then final allocation of money. I hope that some of the great investigators can get funding quickly for their projects.

EV Med Research is a privately-funded R&D laboratory whose mission is to define the most common pathogens responsible for CFS and to develop effective treatment strategies for this illness.

Do you have funding for more studies? Whatís the next step for you?

I have funding for our studies at this time. EV Med Research is a privately-funded R&D laboratory whose mission is to define the most common pathogens responsible for CFS and to develop effective treatment strategies for this illness. We will try to define the mechanism of viral persistence and immune response in the stomach tissues, a place we can consistently find the viral protein. We have reproducibly grown the enteroviruses from some of the stomach biopsies with special techniques. We'd eventually like to look at chemicals that can stop viral replication. Weíd like to define the ďviral formĒ that persists in the tissue.

Dr. Chiaís Research Foundation, the Enviromed Foundation, accepts donations. The Enviromed Foundation is focusing on developing diagnostic tests and treatment for chronic fatigue syndrome (ME/CFS). 

To Overview of the Interview / To Part I of the Interview / A Test Requisition Form to have Dr. Chia analyze whether pathogens are present in stomach biopsies gathered during an endoscopy ($250)

 

Reuters) - A common virus may be a major cause of high blood pressure, researchers said on Thursday in a finding that may bring new approach to treating a condition that affects an estimated 1 billion people worldwide.

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


 

While 5,000 viruses have been described, there are millions.  They're ubiquitous.  One common one is the influenza virus, yet many are known to cause the common cold. 

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.


 

Fever



All of us at some point or another have experienced the body aches, chills and accompanying exhaustion that results from a fever. Fever is defined as an elevated body temperature; however, since people's regular (baseline) temperature varies depending on the time of day and weather conditions, what constitutes fever will vary from person to person.

Fever is caused by what is termed as "pyrogens" ("pyro" is Latin for "fire" or "heat," so "pyrogens" literally means "heat-causing" or "fever-causing" agents). Pyrogens can include viruses, bacteria, drugs and fungi, among others. When these substances enter the body, they affect the hypothalamus, the part of the brain responsible for regulating body temperature--essentially the body's thermostat. Therefore, there are several types of fever, depending on the cause: viral, bacterial, fungal, drug and even traveler's fever (when exposure takes place to unfamiliar foods or diseases while traveling).

The thalamus, faced with an invader, raises body temperature in an attempt to fight off the foreign substance and protect the body. Normally, the heightened body temperature will eliminate the problem, but if the temperature goes above 104 degrees F or if the fever lasts more than 7 days and is accompanied by a stiff neck, severe headache, sore throat, vomiting, rash, bloody stool or painful urination, a physician should be contacted immediately. These symptoms can be a sign that the body cannot handle an invader and needs assistance, such as antibiotics