Friday, March 1, 2013

Interview with Vincent Lombardi, Ph.D- Part 2

Many patients have written and asked WPI for further information about the recent study titled, Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins, published online in the journal In Vivo. We asked Dr. Vincent Lombardi, Research Director of WPI, to give us his answers to the following questions.
Are you looking at other patient cohorts or diseases for this finding?
We would like to study MS and/or lupus subjects. We are seeking a collaborator with the proper specimens.

 Is this something my gastroenterologist could test for?
At this moment, it would be premature for a person to ask their gastroenterologist to look for this. Perhaps it might be justified down the road when we have a better understanding of the significance.

 Are you planning on publishing more papers on pDCs?
Currently, pDCs are a primary focus of our research. We are in the process of writing a paper on pDCs and conducting experiments that will likely result in other publications.

 Are you doing any studies on fibromyalgia?
At the moment, we don't have a study protocol for fibromyalgia.

 What other studies are you working on? Preliminary studies are very helpful to the research process; how can I find out more and be a part of them?
We are studying the pathogenesis of ME and Gulf War illness. Each of these studies is multifaceted. To become involved in these studies, an individual would need to first contact our study coordinator, Kellen Jones, at 775-682-8250 or

Friday, February 22, 2013

Interview with Vincent Lombardi, Ph.D. - Part 1

Many patients have written and asked WPI for further information about the recent study titled, Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins, published online in the journal In Vivo. We asked Dr. Vincent Lombardi, Research Director of WPI, to give us his answers to the following questions.
Question: How did this project come about?
Answer: Dr. DeMeirleir and I began our collaboration on this project about 17 months ago, although we have had an excellent collaborative relationship for many years. My interest in the innate immune response and his interest in gut pathology provided a perfect balance to conduct this research.
Question: I believe that this is the first tissue-study done in those with ME.  Why did you choose to use gut specimens for your study?
Answer: Once Dr. DeMeirleir and I were convinced that the original infectious retroviral association was incorrect, we began to explore other possibilities that could account for some of our previous observations. We believed that the gut pathology might account for the systemic inflammation associated with ME.  Additionally, individuals infected with HIV all have gut issues, as do others with diseases that are characterized by neuro-inflammation.  With all the compelling evidence of the involvement of human endogenous retroviruses (HERVs) in inflammatory diseases like MS and lupus, it made sense to us to look in the gut. I have had a long-standing interest in plasmacytoid dendritic cells (pDCs), and once we realized that HERVs expression was present in only one type of cell, it was one of the first cell populations I suspected.
Question: What does this mean for the ME community?

Answer: We intend to take a responsible and optimistic approach to this preliminary finding and follow it up with good, solid science.  For some time, my focus has been on the type I interferon response, in particular interferon producing pDCs, and their role in inflammatory cytokine production. Therefore, identifying HERVs in these cells is encouraging, but we need to do the hard work to understand what role they play.   Identification of abnormalities in pDCs, which are antigen-presenting cells, certainly could be related to the autoimmune-like symptoms associated with ME. Investigating a potential relationship between autoimmunity and ME is worth further study. We intend to perform this work in collaboration with Dr. DeMeirleir and other researchers and physicians, focusing our research efforts towards a better understanding of our findings.

For the March/April issue of In Vivo, please click on the link below

For the direct link to the manuscript, please click here

If you would like to learn more about WPI's research program, please go to


Friday, February 1, 2013

My letter to the FDA regarding Ampligen

Dear Sir or Madam:
As someone who has lived with ME for 25 years this January, I ask you to please approve Ampligen for a subset of severely disabled patients. My experience with Ampligen was challenging, but worth it. Unfortunately, because I had to pay for the cost of receiving this drug and I suffered from other neurological complications, I was not able to continue on Ampligen. Nevertheless, I am extremely grateful that I had the chance to benefit from the many postive effects of Ampligen for over seven years. After several surgeries to remove non-essential organs my doctor felt Ampligen was my only hope, if we were going to stop the destructive disease progression.
By the age of 21, I was wheelchair-bound and unable to feed, bathe or clothe myself most days because of my chronic disease. I was bedridden and cognitively disabled - unable to read without being really confused. I had to have someone take care of me 24 hours a day, 7 days a week until I began taking Ampligen. It took months before I began to respond but once I started to get well again the improvements in my health were life changing. I was able to take care of my most basic needs once more and to begin a therapeutic program of chair yoga, and get to the dinner table most evenings. Within a year, I was driving to and from the grocery store and using a cart to get around. My most severe symptoms of sinus node sickness and gastro paresis improved significantly, so much so, that I no longer had to consider the pacemakers that specialists had recommended. Within two years, I enrolled in a yoga program to educate myself about therapeutic yoga to help others. In my third year, I began teaching gentle yoga two days a week. I was able to travel on an airplane for the first time and to see friends and family I hadn't seen in years. I made a decision to go off of Ampligen for an extended holiday to see if I could stay in remission without the drug and sadly experienced a total relapse of my symptoms. Once I began again, the drug worked quicker the second time around. I began to see improvement cognitively and physically within months.
As with many drugs, there were some downfalls to being on Ampligen. I had to be infused two times a week at a location one hour away from where I lived. It was a process - getting IV fluids days before my infusions. The intial side effects were difficult to handle at first, but I was blessed to have a doctor who was willing to help me with them. Even with these disadvantages, Ampligen gave me a glimpse of what my life could be without severe ME. I believe that Ampligen treatments may have saved my life.
Ampligen is not a cure, but for those who respond to its healing effects it is a life line. These patients deserve a chance at some quality of life. Like me, they have experienced profound improvements in their cognitive and physical abilities. Ampligen can be a life saving drug for others who suffer from severe ME/CFS.
Thank you for allowing me to share my story with you. I hope for the sake of many patients, you will consider approving Ampligen for severely ill patients while other more accessible drugs are being developed.

Former Ampligen Patient

Wednesday, January 30, 2013

ME Lecture by Dr. Kenny De Meirleir at WPI

ME/CFS from Infectious Disease to Autoimmune Disorder


Dr. Vincent Lombardi, WPI Research Director, introduced Dr. De Meirleir as one of the world's foremost experts in ME and primary research collaborator on WPI’s current RO1 federal grant. He also stated that Dr. De Meirleir has authored hundreds of publications and several books on ME/CFS and other medical research topics. Dr. Daniel Peterson, who was in the audience, was also recognized for his outstanding contributions to this field of medicine.


Dr. De Meirleir's talk included years of significant research which is very technical and complicated. Therefore, this review is not meant to be a summary of the underlying science but rather a summary of the practical application of this work. However, we will place a recording of this talk on the WPI website:, as soon as possible for those who are interested in the actual research data.


Dr. De Meirleir presented a comprehensive lecture on the many factors that appear to play a role in the pathophysiology of ME.  In support of his conclusions, he drew information from other well-known researchers in the field including Drs. Chia, Klimas, Peterson, Mella and Fluge, as well as his more recent clinical studies of patients from Belgium and Norway. After the one hour and fifteen minute presentation, interested patients, researchers, doctors, nurses, and medical students were given a chance to ask questions.


Dr. De Meirleir uses a number of diagnostic tests to diagnose his patients’ underlying biological abnormalities and to guide his successful treatment protocols. Biomarkers include abnormally low NK cell number and function, cytokines indicating a shift in the balance of Th1 and Th2 immune responses, up regulation of Th17 immune cells, and abnormal levels of nagalase and elastase activity. He also tests for various active infectious agents including Borrelia, Bartonella, Brucella, mycoplasma, parasites, and various herpes viruses. He stated that environmental and genetic factors contribute to aberrant protein conformation in some patients.  Other diagnostic tests include fecal analysis and tests for levels of LPS or soluble CD14 as an indicator of gut inflammation.


Basic to Dr. De Meirleir’s treatment protocol is a plan that addresses specific dietary restrictions. He reported that many patients are fructose, lactose, casein and/or gluten intolerant. His patients often begin feeling better after eating a diet free of these substances, as they are most likely to cause an inflammatory response. In addition, he includes a fecal microbial analysis to determine whether or not to begin treatment with pulsed antibiotics. Based on the fecal analysis, which indicates whether or not his patients are suffering from a compromised intestinal barrier, he also prescribes specific probiotics, prebiotics such as lactoferrin, and digestive enzymes. When viruses or other pathogens become chronic Dr. De Meirleir prescribes antiviral therapies and/or additional antibiotic treatments.


It is generally accepted knowledge that ME patients have difficulty controlling various herpes viruses and other pathogens, in addition to exhibiting abnormal natural killer cell function. Subsequent searches for immune modulating drugs have included trials of several different products. Gc-MAF is a macrophage stimulating substance that has recently shown great promise.  Dr. De Meirleir highly recommends that patients address any leaky gut issues before beginning treatment with Gc-MAF.  He also mentioned risks that can be associated with this type of treatment.  Risks include a shift to autoimmunity and an immune reconstitution reaction known as IRIS although  none of his patients have developed autoimmune disease as a result of Gc-MAF treatments and less than 20% have experienced IRIS.   Dr. De Meirleir routinely monitors his patients for IRIS cytokines after starting them on very low doses of Gc-MAF, as a method of prevention. Other immune supportive therapies include the use of Kutapression/Hepapressin complex (Nexavir), which has been reported to inhibit EBV and HHV-6, and Isoprinosine for those with low serum uric acid levels. Finally, Rituximab, a B-cell depletion immune therapy, has been used successfully in a small trial of patients with ME by oncologists Fluge and Mella. Because of the delayed therapeutic response of two to seven months, the authors of this study remarked that there is a possibility that ME has an autoimmune component. (Note: These two physicians are now looking for collaborative research sites and additional funding to engage in a much larger clinical trial due to their 67% rate of success.)


Dr. De Meirleir concluded his talk with a detailed slide describing the various pathways that are disrupted in ME and several other autoimmune diseases. He spoke about a continuum of autoimmune diseases including ME, lupus, RA, type 1 diabetes, and remitting MS that involve a dysregulation of two important immunological pathways, 2’-5’OA synthetase and Th1/Th2 immunity.


It was evident from his lecture that the key to Dr. De Meirleir’s success with patients is his recognition of the serious infectious and immunological issues facing those with ME.  His research provides strong evidence for the support of biological testing and treatment.


WPI is thankful to Dr. De Meirleir for his outstanding commitment to this patient population.  We feel fortunate to be able to provide his lecture as part of our mission to support outreach and education. We look forward to sharing more good news with you in the future.



Tuesday, January 22, 2013

Ampligen: A successful drug for the most severe ME patients

The FDA advisory committee met to discuss Ampligen and its use as a treatment for chronic fatigue syndrome, better known as ME/CFS.  Despite hearing testimony from those who had used the drug and experienced its life changing benefits, the FDA committee voted against its approval.  The committee members asked questions that were reasonable in their attempt to understand the disease that this drug was to address.   However, it was obvious from the questions and the responses that there still remains a tremendous gap between what people think they know about chronic fatigue syndrome and the true devastation that this disease often causes its victims.   Given time and research support, we could learn important information about ME/CFS by thoroughly studying the immunological effects of Ampligen treatments.  Results of such valuable research might also put an end to the misplaced emphasis on “fatigue” as the major biomarker for this disease.

The symptom of fatigue is only one of many more serious symptoms that patients with ME/CFS experience.  The word “fatigue” has created a false impression in the minds of most that this disease is simply a result of a lack of wise energy use.    There is also a mistaken belief that if people with ME/CFS weren’t such overachievers, they would be just fine.  Nothing could be further from the truth.  However, because patients experience a profound loss of energy after becoming ill, the company that makes Ampligen chose to use treadmill testing, or VO2 max testing, as an endpoint to show efficacy of the drug. 

This VO2 challenge test measures the body’s maximum ability to use oxygen efficiently when exercising.  It is commonly used to determine a person’s disability with regards to COPD, a chronic lung disease.   COPD is a well known disease that severely impacts a person’s ability to breathe.   No one has ever linked CFS to this lung disease, but studies have shown that patients with ME/CFS suffer from exercise intolerance.   One wonders if the use of this test could have caused confusion on the part of FDA representatives who may not understand why treadmill testing was used as a biomarker for ME/CFS or more importantly as an endpoint for Ampligen.  They may have been surprised to learn that that such a drug works in a disease that has nothing to do with lung capacity or simple deconditioning.  Perhaps, because some patients with COPD improve their VO2 results with exercise, the misconception is that exercise would likewise be a good therapy for those with ME/CFS.   Interestingly, exercise has just the opposite effect on ME/CFS patients.  Those who are ill suffer more severely when they attempt to return to previous levels of activity.

I suspect that there were many factors, other than misunderstanding the true nature of this illness, which led to the decision not to recommend the approval of Ampligen.  One factor might have been that no one has ever fully explained the mechanisms involved in the VO2 deficit found in patients with ME/CFS.  Nor has anyone described the mechanism of repair in those who take the drug.   Perhaps, had there been a detailed explanation for both phenomena, the FDA might have had better support to back a positive recommendation.  Additionally, Ampligen may have had a better chance at approval had there been more expert testimony from the many physicians who have successfully used Ampligen with their most severely ill ME/CFS patients.  

I don’t mean to sound like I agree with the FDA’s decision.  I do not, because I have witnessed first hand how this drug is incredibly successful at bringing sick individuals from the brink of existence back to a productive life again.  I believe that Ampligen can and should be made available to a subset of patients with ME/CFS.  In those with severe nausea, gastro paresis, tachycardia, cognitive impairment, seizures, and other devastating symptoms, it can be a life saver.  To go from a living death to a healthy existence is by no means an easy feat.   The drug works miracles for some and is all that they have to stop their excruciating suffering.   It is no wonder that these patients continue to fight so hard to keep the drug within their grasp. 

Despite the noticeable physical improvements, important questions remain to be answered.  Why hasn’t Ampligen proven to work for a larger subset of patients with ME/CFS?  What other kinds of biological abnormalities beside oxygen/energy deficits are responding to Ampligen?  Is Ampligen impacting an abnormality in the nervous system?  Is Ampligen repairing a dysregulated immune system? Is Ampligen supporting the mitochondria or power houses of the cells?  What are the key biological abnormalities behind the illness, and how are those abnormalities addressed by Ampligen?  Answers to such questions would help us understand the disease better and answer the question of why Ampligen works so well for some, but not others.   

While we must do much more work to assure all patients receive effective medical care, we can learn a tremendous amount from the Ampligen trials. I believe that Ampligen’s success in this patient population is telling us something important about the disease and those who are most susceptible.   We owe it to the patients to find out what that something is.   Despite the fact that we don’t know the exact mechanisms behind this drug’s efficacy, it has proven to be life saving for some, and therefore, it should be made available to those who truly benefit from its healing properties.  

Annette Whittemore