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Chronic Lyme Disease Viral Co-infection
Human Herpes Virus 6 (HHV-6): Fatigue
Its Link to Chronic Fatigue Syndrome, Fibromyalgia, Fatigue, and
Cancer

Human herpesvirus 6 (HHV-6) was first reported in 1986 and has since become one of the most
widespread members of human herpes viruses. It is composed of two closely related variants that share
over 90% of their DNA homology: HHV-6A and HHV-6B.

Although these two variants are closely related, there are still differences in their epidemiology and
pathogenicity. HHV-6B is acquired in early childhood, infecting up to 90% of most populations during
infancy. HHV-6A, on the other hand, is generally not seen until adulthood. The virus is usually found in
saliva and is presumably spread this way as well.

HHV-6 is of greatest concern to those patients who are immunocompromised, in particular, those who
have undergone organ or bone marrow transplants or who are HIV positive and chronic Lyme disease.
People are carriers of this virus from a young age, and is commonly picked up in dare care centers.
How Does HHV-6 Work?
The virus attacks certain cells, including CD4 lymphocytes, natural killer cells, oligodendrocytes, CD8
cells, and microglial cells. HHV-6 is also animmune suppressive virus that also serves to activate other
viruses. It can be latent in cells for long stretches of time, only to bring about infection later on when
reactivated. HHV-6 can persist in salivary glands, the kidneys, and even the brain until activated.


CFS, Fibromyalgia and Autoimmune
Disease Symptoms Linked to HHV-6.
HHV-6 infection has been associated with a range of maladies including Chronic Fatigue Syndrome (CFS.)
Chronic Fatigue patients typically suffer from immunologic abnormalities and neurologic problems. In
one such study, 30% of CFS patients tested positive in an initial screening for HHV-6. Follow-up cultures
in patients who initially tested negative, later proved positive in an additional 20%-40% of cases. Healthy
control patients have not demonstrated positive cultures as described above. The association between
HHV-6 and CFS reaffirms the link between infection and chronic disease.




One study suggests that a "smoldering" central nervous system (CNS) infection may play a role in
conditions that plague millions of Americans. Jikei University Medical School in Tokyo identified a novel
human herpesvirus-6 (HHV-6) protein, “present in Chronic Fatigue Syndrome (CFS) that is a likely
contributor to the psychological symptoms that are so often associated with the disorder. It was also
found that 71 percent of Chronic Fatigue Symptom patients had antibody SITH-1. What is so remarkable
about this discovery is that 53 percent of depression and 76 percent of bipolar disorder sufferers have
the SITH-1 antibody.

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, Parkinson’s, and
Alzheimer’s
Viruses have been implicated in the development of neurodegenerative diseases such as Alzheimer's,
Parkinson’s, and Multiple Sclerosis (MS.) More specifically, neurotropic virus HHV-6 has been clinically
shown to be directly linked to many neurologic problems including encephalitis, mesial temporal lobe
epilepsy, and many others.

Despite the copious research, HHV-6’s route into the central nervous system remains inconclusive.
However, among various brain regions examined, the highest frequency of HHV-6 DNA was 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 Child’s
Acute Lymphoblastic Leukemia
In one case, a child was found to be infected by HHV-6 and just two months later began an acute
lymphoblastic leukemia. This is just another example of the suggestion that viral infections could play a
major causative role in some childhood leukemia.


HHV-6 Attacks p53 giving rise to cancers
The protein p53 is vital for multicellular organisms as it serves to regulate the cell cycle. As a result it is
an important tumor suppressor that helps the body naturally prevent cancer. The p53 is so critically
important because of the incessant exposure our cells face on a daily basis. From toxic chemicals,
viruses, radiation, to an almost endless barrage of others, our cells are continually at risk. And as our
cells go, we go.

If cells are damaged in sensitive areas by these marauders, there can be devastating repercussions. It is
not uncommon to see key regulatory elements damaged and normal cell growth blocked – setting the
stage for irregular growth and a rapid tumor producing result. The tumor suppressor p53 acts as one of
our best defenses in such circumstance as it snaps into action when it detects DNA damage. The
typically low levels of the protein rise and initiate protective measures by binding to sites in the genome
and halts cell division until the damage can be repaired. If it has progressed too far, p53 will initiate


HHV-6Viral Co-infection of Chronic Lyme
Disease: Immunity and Cancer
Implications
While data is difficult to sort out, the more research that is done seems to further support that
additional regulatory influences in cell proliferation and cell death, including cytokines and growth
factors, are definitively altered after viral infections. HHV-6 is often the culprit for such significant and
impactful changes.


Envita’s Fully Engages Chronic Lyme
Disease Complex and Its Dangerous
HHV-6Co-infection
Envita clinical experience in testing chronic Lyme disease patients, Chronic fatigue syndrome and
fibromyalgia 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 contribute toHHV-6and other virus actively replicate.

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. 2004
        Jan; 71(1): 89-96
    •   Secchiero, Paola, et al. HHV-6 Infection in Immunocompromised Patients. Infections in
        Medicine.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.php this source to site
    •   Seror E, DeVillartay P, Leverger G, Lenoir G. SourceService de pédiatriegénérale, hôpital Necker-
        Enfants-Malades, AP-HP, 149, rue de Sèvres, 75743 Paris cedex 15, France
    •   Dr. David Bell in 2008 on research by Dr. L. Flammand to citation Source Laboratory of
        Molecular Virology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
        20892, USA.
    •   Journal of the American Society of Hematology citations for above

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Human herpes virus_6.spin1

  • 1. Chronic Lyme Disease Viral Co-infection Human Herpes Virus 6 (HHV-6): Fatigue Its Link to Chronic Fatigue Syndrome, Fibromyalgia, Fatigue, and Cancer Human herpesvirus 6 (HHV-6) was first reported in 1986 and has since become one of the most widespread members of human herpes viruses. It is composed of two closely related variants that share over 90% of their DNA homology: HHV-6A and HHV-6B. Although these two variants are closely related, there are still differences in their epidemiology and pathogenicity. HHV-6B is acquired in early childhood, infecting up to 90% of most populations during infancy. HHV-6A, on the other hand, is generally not seen until adulthood. The virus is usually found in saliva and is presumably spread this way as well. HHV-6 is of greatest concern to those patients who are immunocompromised, in particular, those who have undergone organ or bone marrow transplants or who are HIV positive and chronic Lyme disease. People are carriers of this virus from a young age, and is commonly picked up in dare care centers.
  • 2. How Does HHV-6 Work? The virus attacks certain cells, including CD4 lymphocytes, natural killer cells, oligodendrocytes, CD8 cells, and microglial cells. HHV-6 is also animmune suppressive virus that also serves to activate other viruses. It can be latent in cells for long stretches of time, only to bring about infection later on when reactivated. HHV-6 can persist in salivary glands, the kidneys, and even the brain until activated. CFS, Fibromyalgia and Autoimmune Disease Symptoms Linked to HHV-6. HHV-6 infection has been associated with a range of maladies including Chronic Fatigue Syndrome (CFS.) Chronic Fatigue patients typically suffer from immunologic abnormalities and neurologic problems. In one such study, 30% of CFS patients tested positive in an initial screening for HHV-6. Follow-up cultures in patients who initially tested negative, later proved positive in an additional 20%-40% of cases. Healthy control patients have not demonstrated positive cultures as described above. The association between HHV-6 and CFS reaffirms the link between infection and chronic disease. One study suggests that a "smoldering" central nervous system (CNS) infection may play a role in conditions that plague millions of Americans. Jikei University Medical School in Tokyo identified a novel human herpesvirus-6 (HHV-6) protein, “present in Chronic Fatigue Syndrome (CFS) that is a likely contributor to the psychological symptoms that are so often associated with the disorder. It was also found that 71 percent of Chronic Fatigue Symptom patients had antibody SITH-1. What is so remarkable about this discovery is that 53 percent of depression and 76 percent of bipolar disorder sufferers have the SITH-1 antibody. 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, Parkinson’s, and Alzheimer’s
  • 3. Viruses have been implicated in the development of neurodegenerative diseases such as Alzheimer's, Parkinson’s, and Multiple Sclerosis (MS.) More specifically, neurotropic virus HHV-6 has been clinically shown to be directly linked to many neurologic problems including encephalitis, mesial temporal lobe epilepsy, and many others. Despite the copious research, HHV-6’s route into the central nervous system remains inconclusive. However, among various brain regions examined, the highest frequency of HHV-6 DNA was 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 Child’s Acute Lymphoblastic Leukemia In one case, a child was found to be infected by HHV-6 and just two months later began an acute lymphoblastic leukemia. This is just another example of the suggestion that viral infections could play a major causative role in some childhood leukemia. HHV-6 Attacks p53 giving rise to cancers The protein p53 is vital for multicellular organisms as it serves to regulate the cell cycle. As a result it is an important tumor suppressor that helps the body naturally prevent cancer. The p53 is so critically important because of the incessant exposure our cells face on a daily basis. From toxic chemicals, viruses, radiation, to an almost endless barrage of others, our cells are continually at risk. And as our cells go, we go. If cells are damaged in sensitive areas by these marauders, there can be devastating repercussions. It is not uncommon to see key regulatory elements damaged and normal cell growth blocked – setting the stage for irregular growth and a rapid tumor producing result. The tumor suppressor p53 acts as one of our best defenses in such circumstance as it snaps into action when it detects DNA damage. The typically low levels of the protein rise and initiate protective measures by binding to sites in the genome and halts cell division until the damage can be repaired. If it has progressed too far, p53 will initiate HHV-6Viral Co-infection of Chronic Lyme Disease: Immunity and Cancer Implications While data is difficult to sort out, the more research that is done seems to further support that additional regulatory influences in cell proliferation and cell death, including cytokines and growth
  • 4. factors, are definitively altered after viral infections. HHV-6 is often the culprit for such significant and impactful changes. Envita’s Fully Engages Chronic Lyme Disease Complex and Its Dangerous HHV-6Co-infection Envita clinical experience in testing chronic Lyme disease patients, Chronic fatigue syndrome and fibromyalgia 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 contribute toHHV-6and other virus actively replicate. 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. 2004 Jan; 71(1): 89-96 • Secchiero, Paola, et al. HHV-6 Infection in Immunocompromised Patients. Infections in Medicine.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.php this source to site • Seror E, DeVillartay P, Leverger G, Lenoir G. SourceService de pédiatriegénérale, hôpital Necker- Enfants-Malades, AP-HP, 149, rue de Sèvres, 75743 Paris cedex 15, France • Dr. David Bell in 2008 on research by Dr. L. Flammand to citation Source Laboratory of Molecular Virology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. • Journal of the American Society of Hematology citations for above