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Dharam  Ablashi Human Herpes Virus 6A (HHV-6 A) CFS/ME

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Dr Dharan Ablashi HHV-6A CFS/ME

In an article in the Journal of Clinical Virology (in press), Dr. Dharam Ablashi, one of the world's leading experts on HHV6, concludes that CFS (ME/CFIDS) patients are acquiring HHV-6A as a primary infection as adults and not reactivating it from childhood as many have hypothesized.

He also found that the infection has been shown to downregulate the central nervous system, the cardiac system, and the cerebral systems. While variant B was found to be the culprit in multiple sclerosis, variant A was doing the damage in CFS and is found in similar numbers as affects those with AIDS (70%). Reporting on his newest discoveries at the New Jersey CFSA Conference, he said, despite prior reports to the contrary, there were no (0%) controls found with the infection of the A strain, although some healthy controls were found to have the B strain.

Dr. Ablashi did the work by short-term culturing, PCR or RNA for the PCR, and IGM in antibody serum and plasma and found HHV7 was not found, but there was no doubt about HHV-6A being the culprit in the majority of patients tested. Many hypothesis have been proposed. While he cannot rule out Epstein-Barr Virus (EBV), he has done work looking for an enterovirus along with Dr. Robert Gallo and found none. This hypothesis was mainly promoted by Dr. Peter Behan. In 1991, Dr. Elaine DeFreitas found evidence of this but the CDC couldn't replicate her work. He mentioned that they had used a different probe which made their evidence useless. Dr. John Martin claimed to have discovered a spuma virus as causative, but Dr. Jay Levy "failed to be able to support his work. Then, later on, when CFS patients and healthy controls were tested, Martin could not tell the difference." Martin's novel "stealth" virus, he reported, belongs to the same HHV6 and 7 category. The same strain found in AIDS is found in ME/CFIDS. Others have come up with the same scenario such as Zorzeinon from Italy who found 65% had active HHV6. Buchwald, et al found that 70% of the Lake Tahoe patients had an active HHV6A strain. (Ann Intern Med 1992; 116) He has tested Ampligen patients before they took Ampligen and afterward and found the HHV6 had disappeared which "suggests Ampligen can block HHV6." He is now seeing if the same can be found with ganciclovir. Blocking it may not be permanently killing the virus. It may also be activating B cells that only make the condition worsen once you go off the drug. ¯


Dharam V. Ablashi     8 - 12 viruses and CFS

My name is Dharam V. Ablashi.  I am presently the Scientific Director of the HHV‐6 Foundation which
supports research on the role of virus in chronic diseases including Chronic Fatigue Syndrome. I am also
the co‐founder of AACFS and for many years, I served on the Board of Directors of AACFS. I was also the
President of IACFS in 2003‐2004. I served as a senior investigator at NIH/NCI for 22 years where I
conducted research on establishing primate models for lymphomas induced by herpesviruses. In 1986,
while at NCI, I co‐discovered HHV‐6.

The role of microbes in the pathogenesis of CFS has not been explored fully because of the lack of
extramural funding from NIH and CDC. In my opinion, the etiology of CFS is multi‐faceted. While
infection may not trigger the illness in all cases, I have long believed that the evidence indicates
infectious agents are involved in many cases. Indeed, the literature documents clearly that CFS can
follow in the wake of infection with Epstein‐Barr virus, human herpesvirus‐6, Ross River virus, B.
burgdorferi (the cause of Lyme disease), C. burnetii (the cause of Q fever), parvovirus B19, the
enteroviruses and possibly mycoplasma organisms.
I am sorry to say that, over the years, several people in leadership positions both at the NIH and CDC
have made it clear that they do not believe that studying infectious agents in CFS is important, and thus
it has been neglected. This issue has become urgent with the recent report that a retrovirus (XMRV) is
found in many patients with CFS, and in few healthy controls, published in Science from the
Whittemore‐Peterson Institute (2009). Given the known tropism of retroviruses, XMRV is an entirely
plausible candidate to be producing the well‐documented abnormalities of the central and autonomic
nervous system, of the immune system, and of energy metabolism. Moreover, it is entirely plausible
that XMRV may reactivate latent infectious agents—particularly the herpesviruses and endogenous
retroviruses—which then contribute to producing pathology.

The CDC has made several assumptions that we believe will prove to be in error:
1. The CDC has assumed that if a pathogen exists, it can be found in the serum, and
2. The CDC assumed that if there is a pathogen, it is only one pathogen, not 8‐12 pathogens that
cause variations of the same syndrome.
3. The CDC has assumed that the timing of sample collection is unimportant
We think it is likely that CFS is a heterogeneous disorder and that there are multiple factors and
pathogens that contribute to the condition. Even if XMRV is found in the majority of CFS patients, we
expect that there are at least 8‐12 other pathogens that act as co‐factors to cause pathology. Unless you
are looking for subsets, infections such as parvovirus B‐19 or Q fever (which might represent a small
fraction of the cases) will be completely overlooked as unimportant. Statistically, none of the subsets
may be statistically significant, but when added together, these subsets could be very important.
Patient samples from newly diagnosed cases of CFS offer the best chance of finding evidence of an
infectious agent. Studies should be organized to examine samples from these patients separately from
those who have been ill for decades.

Much provocative work on infectious agents and CFS has languished for lack of funding. For example,
Brigitte Huber at Tufts found that EBV could activate HERV‐K18, an endogenous retrovirus. Danish
investigator Per Hollsberg from University of Aarhus found that HHV‐6 activates HERV‐K18 as well. Dr.
Jose Montoya at Stanford University found marked clinical improvement when patients with CFS and
active infection with EBV and/or HHV‐6 were treated with an antiviral. Professors Ron Glaser and Nancy
Klimas showed that EBV‐DUTpase, a nonstructural protein, could activate NF‐KB resulting in the
production of proinflammatory cytokines which contribute to the pathophysiology associated with
disease. Using biopsy specimens, Dr. John Chia at EB Medical Research in California has documented the
presence of enterovirus in stomach antrum endothelium in 82% of stomach biopsies from patients with
CFS compared to 20% of controls. Parvovirus B‐19 has been implicated in a subset of CFS patients by
several investigators, and new cardiac biopsy data from Europe suggests that the pathology may be due
in part to chronic infection of myocardial tissues. Furthermore, Q‐Fever is the cause of CFS in some cases
and it is often missed by physicians outside of the US.

It is imperative that the CDC study biopsy samples from the gut, and brain as well as heart tissues, and
that they look at spinal fluid. Most of the studies done by the CDC have been on serum. However, many
pathogens cannot be found in the serum because they do not circulate in the peripheral blood after the
initial infection. For example, Dr. Steven Jacobson’s team at NIH has found a high viral load of HHV‐6 in
the brain tissue biopsies from mesial temporal lobe in epilepsy patients, even though serum and spinal
fluid were negative for the virus. They also found that HHV‐6 is barely detectable in the spinal fluid,
even after full‐blown HHV‐6 encephalitis. A virus such as HHV‐6 can persist in the brain tissue in spite of
completely normal antibody levels in the peripheral blood. Of course it is far more convenient to look
for virus in the serum. In this case, however, the only way to determine if these pathogens are
responsible for central fatigue is dig deeper and start testing the brain tissue itself.
In summary, we propose that CDC should invest the majority of its research budget into exploring
pathogens in CFS, with particular emphasis on examining spinal fluid, brain tissue, cardiac tissues and
gut biopsies. I am confident this area of research would be beneficial to the health of CFS patients.

Herpes Virus Expert Sheds Light on Chronic Fatigue Syndrome Mysteries

by John W. Addington
May 2, 2003

Dharam V. Ablashi, DVM, MS, Dip.Bact., co-discoverer of unusual "juicy" white blood cells and current American Association of Chronic Fatigue Syndrome President, has done much to advance the understanding of the cause of Chronic Fatigue Syndrome (CFS).

Dr. Ablashi has many more credits to his name. He is internationally renowned for his work with herpes viruses and has served on national and international scientific committees including NIH and W.H.O. He is Director of the Herpesvirus Programs at Advanced Biotechnologies Inc, and Adjunct Professor of Microbiology at the Georgetown University School of Medicine in Washington, D.C. Furthermore, Dr. Ablashi has shared in the publishing of over 285 scientific papers, 11 books, and he has lectured worldwide.

However, it is Ablashi's research regarding human herpes virus 6 (HHV-6) particularly that has involved him with Chronic Fatigue Syndrome.

Ablashi was working with the National Cancer Institute in the mid-80's when he and his associates discovered odd balloon-shaped white blood cells which they described as “juicy.” These researchers published their findings about this new virus in 1986. Later they confirmed this was a herpes virus, and as it was the sixth such virus to be discovered it was called human herpes virus 6.

Other Herpes Viruses

Other herpes viruses are involved in cytomegalovirus, chickenpox, infectious mononucleosis, herpes simplex, and shingles. The herpes virus that causes mononucleosis, Epstein-Barr virus, also know as HHV-4, was initially suspected as a cause of CFS. Ablashi has done research on this virus also and he published in 1995 that "the involvement of Epstein-Barr virus in CFS patients is diminishing." Nevertheless, he stated that there could "be a subset of CFS patients in whom Epstein-Barr virus may be a major contributing factor to disease manifestation."


As a childhood infection, HHV-6 can cause the rash-like condition roseola. Dr. Ablashi explains that, "HHV-6 infection usually occurs in childhood during the first year of life and then the virus becomes latent." HHV-6 has two forms designated as HHV-6A and HHV-6B. It is HHV-6B that is associated with roseola and over 90% of adults retain this virus dormant in their system throughout their lives. Ablashi states that "variant A is more common in AIDS patients and patients with CFS."

As the research developed with HHV-6, many researchers, including Ablashi, performed studies to determine whether that virus might be the cause of CFS. These studies, while not always consistent, have often found a majority of CFS patients show signs of recurrent HHV-6 infections. This is not so with healthy persons.

In a study published in the Journal of Clinical Virology, Dr. Ablashi and associates looked for unique signs of HHV-6 infection in 35 CFS patients. While dormant, HHV-6 can be detected in most adults. These researchers studied immune system markers that would detect reactivation or possibly active HHV-6 infection.

Among the CFS patients, 54% showed evidence of HHV-6 reactivation whereas this was only true in 8% of the healthy individuals. Further testing over a two and a half year period revealed two subsets of CFS patients had persistent HHV-6 infection. Ablashi and his co-authors wrote that these results "show a significantly high frequency of HHV-6 reactivation in CFS patients…and a decrease in cellular immune responses."

Hormone Imbalance and HHV-6

Neuroendocrine function has often shown to be imbalanced in CFS patients. Neuroendocrine refers to the brain's control of proper hormone balance for good health. Thus the question arises as to how this relates to Ablashi's research on HHV-6.

Dr. Ablashi offered this explanation. "First, the data generated by us clearly show that HHV-6 variant A is present in the cerebral spinal fluid of most, but not all, CFS patients. The virus seems, therefore, to be carried to the central nervous system (CNS) via [white blood cells], where it has been found to be latent. When the [white blood cells] come in contact with [brain] cells/tissues, somehow the virus becomes activated, spreads to the CNS and induces CNS manifestations. …This may be a method in which HHV-6A participates in neuroendocrine dysfunction."

HHV-6 Treatment

When asked about the potential treatment of HHV-6 infection for those with CFS, Dr. Ablashi offered some insightful comments. He states, "Dr. Daniel Peterson, with whom I collaborated on a CFS project, tried ganciclovir, foscarnet and Ampligen in his CFS patients, who were identified by us and two other labs, to contain active HHV-6 infection."


"Four patients treated with ganciclovir showed the presence of HHV-6A, even after anti-viral treatment. Only one patient improved slightly for a short while."


"Two patients treated with Ampligen improved initially and did make remarkable recoveries. When treatment was discontinued after 1 1/2 years, however, HHV-6A was found to be activated from latency and these patients started to show signs of the illness."


"The patient treated with foscarnet improved greatly since he returned to work on a full time basis. We found no HHV-6A infection after foscarnet treatment. Another CFS patient treated elsewhere with foscarnet also improved greatly and returned to college. In her case, the viral DNA copies in the plasma and CNS after treatment were greatly reduced. Foscarnet, therefore, is quite effective in suppressing HHV-6A infection, but it is also associated with toxicity. Most physicians, because of this, are not willing to experiment with it."

Whey Protein Combined with Foscarnet

Patients considering foscarnet may be interested in research by Dr. Ablashi which tested the drug's effectiveness in combination with whey protein. Ablashi found that when used in combination with foscarnet, the effect is greater than each has individually.


Both through his ongoing research and his work with the American Association of Chronic Fatigue Syndrome, Dr. Ablashi has extended himself on behalf of those with CFS. And for that, the CFS community applauds him.

For assistance with issues related to CFS and HHV-6, Dr. Ablashi can be contacted through: The American Association of Chronic Fatigue Syndrome, online at
E-mail:; Voice mail: 206-781-3544.

Dr Alblashi HHV-6 Foundation
The HHV-6 Foundation is also engaged in finding and/or developing effective antiviral agents. Progress in this area has been slow; they have checked out over 60 compounds, only two of which (red marine algae, amantadine) have worked in more advanced testing. Dr. Ablashi noted, however, a variety of antivirals (ampligen, Isoprinosine, alpha 2a interferon (?), acyclovir, valcyclovir, valganclyclovir) that have been successful in small trials. Three of these will be covered in the Clinical trials session of the conference.

Susan Levine. Incidence of HHV-6 and EBV infection in Chronic Fatigue Syndrome patients.

The herpesviruses have long been of interest in CFS. Several researchers believe that EBV and HHV-6 reactivation plays an important role in a subset of CFS patients. Questions regarding proper diagnostic procedures have, however, muddied this issue considerably. Dr. Levine’s study was designed to bring some clarity to this issue.

Dr. Levine employed a variety of different tests (EBV, HHV-6 – IgG, IgM, PCR; EBV – viral capsid antigen (VCA), early antigen (EA), EBV nuclear antigen (EBNA); HHV-6 – antigenemia), to determine if HHV-6 and EBV reactivation was present in CFS patients, and if it was, to determine the best means of testing for it.

She found that CFS patients tested normally to two common antibody tests (VCA, EBNA) but that about a third of CFS patients – compared to zero controls – tested positive for high levels of antibodies to EBV’s early antigen (AG). About a third of the CFS patients also exhibited elevated levels of antibodies to HHV-6 and about 20% were positive in the HHV-6 antigenemia tests vs. zero controls.

PCR tests of the blood lymphocytes indicated that the CFS patients all harbored the HHV-6A virus while the controls harbored the HHV-6B virus. Several researchers believe that not only are these different viral types but they are completely different viruses and should be denoted as such. (See HHV-6 and CFS).

Dr. Levine’s study, then, presented evidence that a substantial subset of CFS patients have an active chronic low level herpesvirus infection. Antibody tests suggest that HHV-6A is active and replicating in about 30% of CFS compared to zero controls. EBV replication, on the other hand, does not appear to be occurring. Instead this study appears to back up Dr. Glaser’s theory that EBV is active enough in CFS to produce immune system altering proteins but is shut down before it can replicate.


Chronic Fatigue Syndrome (ME/CFS) Studies - Amantadine was poorly tolerated by ME/CFS patients and showed little benefit in a cross-over study with carnitine.

Chronic Fatigue Syndrome (ME/CFS) Doctors Report - Over a small sampling of patients Dr. Bell found that 40% could not tolerate the drug (mostly due to jitteriness and anxiousness) and 40% reported from moderately improved to excellent results. Amantadine seemed to be most effective in treating moderately ill patients. Dr. De Meirleir reports Amantadine relieves fatigue in some ME/CFS patients.

Recent research by others has shown that amantadine successfully inhibits Borna disease virus (BDV) in both cultured cells and in an infected human. Among the CFS patients we studied, some had antibodies against BDV in their plasma and BDV RNA in their blood. One group of these patients, from a single family, began using amantadine and found improvement in their CFS symptoms.

To further investigate this dymanic, we administered amantadine to 22 patients with CFS. Three patients withdrew from the study because of side-effects from the treatment. The other 19 took 200 mg per day of amantadine for eight weeks. When we evaluated the effects of the substance on patients with and without antibodies against BDV in their plasma, 6 of 11 patients with BDV antibodies showed a good response, whereas only 2 of 6 patients without the antibodies showed improvement.

There have been many conflicting reports about the effectiveness of amantadine on BDV. So the mechanism of the effect of this substance is unclear, but we consider it one of a range of therapies for some CFS patients

Amantadine and L-carnitine treatment of Chronic Fatigue Syndrome.

Carnitine is essential for mitochondrial energy production. Disturbance in mitochondrial function may contribute to or cause the fatigue seen in Chronic Fatigue Syndrome (CFS) patients. Previous investigations have reported decreased carnitine levels in CFS. Orally administered L-carnitine is an effective medicine in treating the fatigue seen in a number of chronic neurologic diseases. Amantadine is one of the most effective medicines for treating the fatigue seen in multiple sclerosis patients. Isolated reports suggest that it may also be effective in treating CFS patients. Formal investigations of the use of L-carnitine and amantadine for treating CFS have not been previously reported. We treated 30 CFS patients in a crossover design comparing L-carnitine and amantadine. Each medicine was given for 2 months, with a 2-week washout period between medicines. L-Carnitine or amantadine was alternately assigned as fist medicine. Amantadine was poorly tolerated by the CFS patients. Only 15 were able to complete 8 weeks of treatment, the others had to stop taking the medicine due to side effects. In those individuals who completed 8 weeks of treatment, there was no statistically significant difference in any of the clinical parameters that were followed. However, with L-carnitine we found statistically significant clinical improvement in 12 of the 18 studied parameters after 8 weeks of treatment. None of the clinical parameters showed any deterioration. The greatest improvement took place between 4 and 8 weeks of L-carnitine treatment. Only 1 patient was unable to complete 8 weeks of treatment due to diarrhea. L-Carnitine is a safe and very well tolerated medicine which improves the clinical status of CFS patients. In this study we also analyzed clinical and laboratory correlates of CFS symptomatology and improvement parameters.
Dr Myhill: Acumen laboratories now routinely check A-L-carnitine levesl for me and they are almost always low in CFSs.


This phosphonic acid derivative (marketed by Clinigen as foscarnet sodium under the trade name Foscavir) is an antiviral medication used to treat herpes viruses, including drug resistant cytomegalovirus (CMV) and herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2). It is particularly used to treat CMV retinitis. Foscarnet can be used to treat highly treatment experienced patients with HIV as part of salvage therapy.[1][2][3]

Mechanism of action

Foscarnet is a structural mimic of the anion pyrophosphate[4] that selectively inhibits the pyrophosphate binding site[citation needed] on viral DNA polymerases at concentrations that do not affect human DNA polymerases. Because foscarnet is not activated by viral kinases it maintains activity against viruses like HSV and VZV that have respectively developed mutant thymidine kinase and UL97 encoded protein kinase, to gain resistance to other DNA polymerase inhibtors, like acyclovir and ganciclovir. Therefore, foscarnet is often used in acyclovir- or ganciclovir-resistant disease.

However, acyclovir- or ganciclovir-resistant mutants with alterations in viral DNA polymerase may be resistant to foscarnet.[5][6]

Administration Intravenous only

Side effects

Nephrotoxicity - Increase in serum creatinine levels occurs on average in 45% of patients receiving foscarnet. Other nephrotoxic drugs should be avoided. Nephrotoxicity is usually reversible and can be reduced by dosage adjustment and adequate hydration.
Electrolyte disturbances - Changes in calcium, magnesium (Harisson 16th ed page2244) potassium and phosphate levels occurs commonly and regular monitoring of electrolytes is necessary to avoid clinical toxicity.
Genital ulceration - Occurs more commonly in men and usually occurs during induction use of foscarnet. It is most likely a contact dermatitis due to high concentrations of foscarnet in urine. It usually resolves rapidly following discontinuation of the drug.
CNS - Paraesthesias,irritability and hallucinations


In Development

Artesunate - Artesunate is a well tolerated drug approved for malaria (in Europe) that possess antiviral activity as well. In vitro (lab) studies found it was highly effective against one of HHV-6’s cousins; the cytomegalovirus.

An HHV-6 Foundation funded study indicates artesunate also effectively inhibits HHV-6A in the lab. This drug is particularly promising because, in contrast to ganciclovir and foscarnet, it hits HHV-6 early in its life cycle. If HHV-6 produces a kind of smoldering infection that alters cell functioning in ME/CFS and other diseases then hitting it early will be critical. What a boost it would be to find an already approved drug that was effective against HHV-6.

Cycloprovir – analogue of ganciclovir but potentially much more effective against HHV-6. (Valcyte converts to ganciclovir in the body. Ganciclovir interferes with viral replication.

CMX001 – a variant of Cidofovir – is highly effective again many DNA viruses and is 3x’s better than Cidofovir against all herpes viruses in the lab. Its antiviral activity in animal models is very good as well. In the first clinical study it was well tolerated.

CMV423 – a new compound very effective against HHV-6 and cytomegalovirus

HPMP-5-azal – Six times more effective against HHV-6 than Cidofocir. Much more efficient and much less of the drug is needed. This is important because toxicity is a big problem with cfidovir. Possibly a big hit.

Marabavir (MBV) – inhibits cytomegalovirus replication. Currently in Phase III trials. Good against EBV. Contrary to previous reports, possibly good against HHV-6. About 50-100 times more efficient than cidofovir in some tests.

Arysulfone derivatives – good antiviral activity, among most potent of anti-virals.

Indication of prices for virus tests in serum.

But viruses should be searched in spinal fluid, brain tissue, cardiac tissues and
gut biopsies and not in serum.

Herpes viruses 8 species 50 - 100 usd per species 400 - 800 usd -ebv
Epstein-Barr Virus (EBV) 200 - 600 usd
adeno-viruses 500 - 12.000 usd microbix
coxsackie viruses  500 - 800 usd
cytomegalic virus (CMV) 70 - 150 usd
enteroviruses 150 usd
Spuma Virus
retrovirus 60 and up


CFS and Virusses

Epstein-Barr Virus (EBV)
coxsackie viruses
cytomegalic virus (CMV)
Spuma Virus

Feel tired all of the time? Still feel tired after sleeping? Always having trouble sleeping? These are serious signs of sleeping disorder problems. Sleep disorder doctors like Dr. Mazlen can prescribe fibromyalgia medicine or treatments that can help you overcome these issues and avoid the risk factors.

Infectious disease states can be associated with fatigue of varying degrees. Chronic bacterial infections associated with continuous debilitating fatigue are uncommon since the advent of modern antibiotic therapy. Unfortunately, there is a much smaller drug-armentarium to be used against viruses and organisms such as the causative agent in Lyme's disease. Post-viral fatigue syndromes, however, are seen commonly after a variety of viruses, the best-known of which is Epstein-Barr Virus (EBV), or the cause of the common variety of infectious mononucleosis. The term infectious mononucleosis syndrome was coined in medical literature in 1920. Since that time a wide-ranging variety of viruses is known to cause an infectious mononucleosis syndrome. Some examples of such viruses are adeno-viruses, coxsackie viruses, cytomegalic virus (CMV) and a variety of enteroviruses. Some authorities view CFIDS, or CFS, as a chronic viral reactivation syndrome (See Table 1 for a pathophysiology of CFS). There is a great deal of controversy currently as to how many viruses may be involved, and teams of suspect-viruses have been postulated with some cases suspected to have 5 or more viruses possibly interacting to cause clinical CFIDS. Even animal viruses such as the Spuma Virus are under clinical investigation. In some cases, a retrovirus similar to HLTV-2 appears to play an important role, especially where the central nervous system has been damaged and neurologic symptoms are prominent.

A first diagnostic approach to ascertain if an individual has CFIDS, or CFS, must include a work-up or diagnostic evaluation to exclude other important or serious causes of chronic fatigue such as: anemia, arthritic diseases, cancer, collagen-vascular diseases such as lupus erythematosis, acute or chronic Lyme's Disease, inflammatory bowel diseases, malnutrition and malabsorptive states, parasitic infections and finally, of course, AIDS.

Once this type of complete clinical evaluation has excluded the above types of fatigue causes, although any of these can and often does coexist with CFIDS, then the current clinical state of the individual must be ascertained by physical and laboratory evaluation. It isn’t unusual to find that as a result of viral activity or infection there may be inflammatory disease of the muscles, tendons, joints, liver, pancreas, thyroid, central nervous system and also of the gastrointestinal tract, including the stomach, small bowel and colon.

Also, in as many as 50% or more of CFIDS sufferers, there is an exacerbation , or flare-up of allergies (Strauss and others see bibliography**). Mild or borderline allergies may become moderate to severe in nature, and asthma can become active or, if already present, can become more severe.

Clearly, as previously outlined, the individual with CFIDS, or CFS, can be seriously or severely ill, and total disability is not uncommon for some period of time. Some cases suffer a more on-and-off clinical course.

The challenge to the treating physician is a therapeutic one. In over ten years of treating such cases, Dr. Mazlen’s approach is complimentary in nature; it includes diet and nutritional interventions, medical, nutritional and/or drug therapy for the complications that occur, life-style adjustments, therapeutic exercise and stress management.

It should be emphasized that stress can reactivate Epstein-Barr Virus (EBV) (see paper of Ronald Glaser and others in Dr. Mazlens’s bibliography**). In their study, even examination stress among medical students could trigger measurable EBV (latent) reactivation. Dr. Mazlen’s experience is that all varieties of stress; emotional, physical and socioeconomic, are associated with relapses which can be mild to severe in degree.

It is the overall impression that successful treatment of the individual with CFIDS, or CFS, must be the treatment of the whole person in context with his or her total environment. This is the philosophy that guides Dr. Mazlen’s treatment programs, which includes nutritional support, drug therapy, psychological support groups, exercise programs and IV treatments such as gamma-globulin and others.

There are several researchers currently investigating the possibility of other novel or new viruses in the causation of CFS. Some viruses under investigation are the Spuma Virus and a mystery AIDS-like virus.

More recently in the 1990’s, attention has been drawn to another family of viruses as a cause of post-viral fatigue syndrome, and possibly a cause of CFIDS as well; namely, the coxsackie virus. British Scientists and medical researchers in England discovered coxsackie viruses to be the cause of a mid-1980’s epidemic of post-viral fatigue syndrome. Previously known and studied, this family of enteroviruses had been shown to cause meningitis, myocarditis, pericarditis, pleurisy, pleuritis, hepatitis and pancreatitis among other disease states. Some of the various A and B serotypes of this enterovirus family have more characteristic disease-state profiles, but what is important to the understanding of CFIDS is their ability to produce viral persistance in an infected host, and thus to cause chronic, relapsing disease states in humans. (Table 3 bottom of page)

Coxsackie B virus has been implicated in widespread or localized myalgia, also known as Bornholm Disease, which was first described in the late 1800’s, characterized by fever and chest and/or abdominal pain. This form of epidemic pleurodynia has been prevalent in the greater metropolitan New York region for over 2 years. The emerging picture stemming from this regional epidemic included numerous cases of both coxsackievirus mononucleosis (or post-viral fatigue syndrome) and exacerbated or relapsing CFIDS. The importance of being aware of this possible contribution of apparent CFS cases is that coxsackievirus B (post-viral syndrome) may persist anywhere from 2 months to 2 years independent of what other concomitant infectious diseases may be present. Most often, persistent coxsackievirus B infection affects muscles, reduces exercise tolerance and causes muscle pain commonly referred to as myalgia, and can be a cause of fibromyalgia rheumatica.