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    Chronic Fatigue causing Virus (HHV-6)

    Human Herpes Virus 6 linked to Chronic

    Lyme disease:Its Link to Chronic Fatigue Syndrome, Fibromyalgia, Fatigue, and

    Cancer

    First reported in 1986, human herpesvirus 6 (HHV-6) has since become one of the most widespread

    members of human herpes viruses and comes in two related variants: HHV-6A and HHV-6B. And though

    similar, there areclear differences in their epidemiology and pathogenicity.

    HHV-6B is acquired in early childhood (often in daycare centers) and is responsible for infecting up to

    90% of most populations during infancy. HHV-6A behaves quite differently as it is generally not seenuntil adulthood. Both versions of the virus can be found in saliva and are presumably spread this way as

    well.

    The HHV-6 virus is of greatest concern to immunocompromised patients. Among those at the greatest

    risk of severe HHV-6 complications are those who have undergoneorgan or bone marrow transplants or

    who are HIV positive and those with chronic Lyme disease.

    http://www.envita.com/conditions-we-treat/lymedisease/http://www.envita.com/conditions-we-treat/lymedisease/http://www.envita.com/conditions-we-treat/lymedisease/
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    How Does HHV-6 Work?

    HHV-6 is known to attack specific cells including but not limited to CD 4 lymphocytes, NKTs,

    oligodedrocytes, CD8 cells, and microglial cells. Moreover, this virus is immune suppressive and also

    activates other viruses in the process. While HHV-6 can remain latent for long periods of time, it can

    reactivate and cause infection quickly. The virus can lie in wait in the salivary glands, kidneys, or brain

    until reactivated.

    CFS, Fibromyalgia and Autoimmune

    Disease Symptoms Linked to HHV-6

    Maladies resultant of HHV-6 are many, and includes the idiopathic illness Chronic Fatigue Syndrome

    (CFS). Patients who suffer with CFS potentially face immunologic abnormalities and neurologic

    problems. It was observed in one study that 30 percent of CFS patients tested positive for HHV-6 and

    after a series of follow-up tests, it was discovered that an additional 20-40 percent were also positive

    after initially showing no trace of the virus. The obvious association between HHV-6 and CFS reaffirms a

    much broader link between infection and chronic disease.HHV-6 is one of the infections found invirtually

    all Chronic Lyme Disease patients a chief contributor to fatigue and other neurological symptoms.

    Antibiotics do not affect this or other herpetic viruses.

    HHV-6 as a Potential Causative to

    Chronic Lyme Disease, Parkinsons, and

    Alzheimers

    Neurodegenerative diseases such as Alzheimer's, Parkinsons, and Multiple Sclerosis (MS) look

    increasingly appear to be catalyzed by viral infections. More specifically, neurotropic virus HHV-6 has

    been clinically shown to be tied to many neurologic problems including encephalitis, mesial temporal

    lobe epilepsy, and many others.

    Nevertheless, HHV-6s route into the central nervous system remains inconclusive. However, among

    various brain regions examined, the highest frequency of HHV-6 DNA can be routinely identified in the

    olfactory bulb/tract region. While further tests must be conducted, the olfactory pathway does seem

    likely as at least one pathway for HHV-6 to move into the CNS.

    HHV-6 Infection: Its Role in One Childs

    http://www.envita.com/chronic-fatigue-syndrome/http://www.envita.com/chronic-fatigue-syndrome/http://www.envita.com/chronic-fatigue-syndrome/
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    Acute Lymphoblastic Leukemia

    In one case, a childs acute lymphoblastic leukemia came only two months after an HHV-6 infection was

    detected.Evidence continues to mount that suggests viral infections could play a major causative role in

    some childhood leukemia.

    HHV-6 Attacks p53 giving rise to cancers

    Protein p53 regulates the cell cycle and thereby serves as an invaluable tumor suppressor one that

    plays a vital role in helping the body prevent cancer development and growth.

    How does p53 work?

    p53 snaps into action when it detects DNA damage. Typically low levels of the protein rise immediately,initiating protective measures by binding to sites in the genome and halting cell division until the

    damage can be repaired. Should the damage have progressed too far for repair, p53 will trigger

    apoptosis, or cell self-destruction, eradicating the problem swiftly and completely.

    HHV-6 Viral Co-infection of Chronic

    Lyme Disease: Immunity and Cancer

    Implications

    Regulatory influences in cell proliferation, studies show, can be altered definitively by viral infections.

    HHV-6 is a common perpetrator for such significant and impactful changes drawing additional attention

    from researchers across the globe.

    Envitas Fully Engages Chronic Lyme

    Disease Complex and Its Dangerous

    HHV-6 Co-infectionEnvita clinical experience in testing chronic Lyme disease patients shows many have activated forms of

    co-infection viruses such as HHV-6. That means that many Lyme sufferers are likely carriers of this

    infection as well as others. Biofilm communities and immunodeficiencies could make HHV-6 and other

    virus actively replicate.

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    Envita employs only the most advanced diagnostic tools to test for a variety of infections like HHV-6, and

    examine whether it is a causative factor for other maladies, such as Chronic Fatigue Syndrome. We

    utilize the most effective therapies from around the world to modulate and boost immune function in

    patients suffering with HHV-6 or those who are immunocompromised and at risk of contracting it.

    References:

    Abel-Haq, N.M. and Asmar BI. Human herpesvirus 6 (HHV-6) infection. Indian J. Pediatr. 2004Jan; 71(1): 89-96

    Secchiero, Paola, et al. HHV-6 Infection in Immunocompromised Patients. Infections inMedicine.2005; 22(3).

    Wisconsin Viral Research Group, Ltd. wisconsinlab.com Institute of Human Virology, University of Maryland, Baltimore, Baltimore, MD, (citations for the

    above)

    http://www.medicalnewstoday.com/releases/112548.phpthis source to site Seror E, DeVillartay P, Leverger G, Lenoir G. SourceService de pdiatriegnrale, hpital Necker-

    Enfants-Malades, AP-HP, 149, rue de Svres, 75743 Paris cedex 15, France

    Dr. David Bell in 2008 on research by Dr. L. Flammand to citation Source Laboratory ofMolecular Virology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland

    20892, USA.

    Journal of the American Society of Hematology citations for above

    http://www.medicalnewstoday.com/releases/112548.phphttp://www.medicalnewstoday.com/releases/112548.phphttp://www.davidsbell.com/LynNewsV5N3.htmhttp://www.davidsbell.com/LynNewsV5N3.htmhttp://www.davidsbell.com/LynNewsV5N3.htmhttp://www.medicalnewstoday.com/releases/112548.php