I had only been in clinical practice for about a year when Incline Village, Nevada became ground zero for chronic fatigue syndrome (CFS). Daniel Peterson and Paul Cheney, both private practice physicians at Incline Village, became pioneers in a shadow epidemic that started with an outbreak of a strange illness in 1984 in the Lake Tahoe region.
Within three years, the two physicians found the illness in 259 patients in the area. Because symptoms were similar to mononucleosis, Peterson and Cheney believed Epstein Barr Virus (EBV) caused it. After a few years, however their theory was proven wrong.
A Real Illness with Many Names
During this same time period, patients started to arrive at my clinic in San Diego with similar complaints: debilitating fatigue, brain fog, and weakness without an infection or obvious underlying illness. What was first suspected as a local epidemic very quickly showed up in other parts of the United States and Europe, mostly in Britain.
Doctors were baffled. In 1987, the New York Times published a long article about the new illness. People were getting sicker without a reason.
More and more cases of CFS, also referred to as “chronic fatigue immune deficiency syndrome (CFIDS)” or “myalgic encephalomyelitis (ME)” in England, turned up. Patients sought treatments that didn’t exist for an illness that wasn’t recognized as a disease. Conventional MDs brushed patients off as hypochondriacs. It was not until 1994 that the CDC recognized CFS as a real condition, giving it an ICD diagnostic code under the “Fukuda definition.”
A Real Diagnosis
Developed by a research team lead by Keiji Fukuda, M.D., M.P.H., an influenza epidemic specialist, for the first time CFS suffers had a real diagnosis to legitimize their condition.
The clinical definition of persisting or relapsing debilitating fatigue contained eight points that included the concurrent occurrence of four or more of the following symptoms:
- Substantial impairment in short-term memory or concentration;
- sore throat;
- tender lymph nodes;
- muscle pain;
- multi-joint pain without swelling or redness;
- headaches of a new type, pattern, or severity;
- refreshing sleep; and
- post-exertional malaise lasting more than 24 hours.
The Disease Hits Me
In 1996, after completing ethnobotanical fieldwork at a biological research station in the upper Amazon rainforest, I was taken by a malaria-like illness. After months of intensive diagnostics, my doctors declared that I didn’t have malaria, but they had no idea what
caused my massive fatigues and weakness, severe joint pain, and inability to think clearly.
I was so exhausted that it took a major effort to even pick up a pencil! I had all eight of the CDC criteria symptoms, and every one was severe. In fact, I was considerably sicker and weaker then most of my CFS patients.
Frustrated with conventional medicine, I eventually treated myself and gradually recovered. But it took years. My experience with CFS inspired me to delve deeper into viral disease, which resulted in the publication of my first book, Viral Immunity, in 2000.
Anti-Viral Drugs Seem to Work
For more than ten years, viral infection as a cause for CFS was ignored. Most of the clinical focus shifted to adrenal fatigue, hormone deficiencies, allergies, and stress-related imbalances.
I wasn’t satisfied with any of the explanations, because they were too easy, not grounded in good clinical science, and the biological understanding of complex immune interrelationship was still in its infancy. And, when patients were treated with therapies for these causes, they still didn’t get better. When treated with common anti-viral drugs used for herpes simplex virus, however, most patients felt distinctively better.
From my view, viral and other infections like mycoplasma that were found in laboratory studies of my CFS patients had something to due with the condition. But were they the cause, or only linked to the disease?
The Science Falls Apart
In 2006, scientists announced a provocative finding about a retrovirus called “xenotropic murine leukemia virus-related virus (XMRV).” A handful of retroviruses, like HIV that causes AIDS, were getting a lot of attention. XMRV, closely related to a known virus from mice, was found to be associated with prostate cancer. In 2009, what was to become one the most interesting and bruising scientific debates of the times came to light: XMRV was thought to be the cause of CFS.
At first, results weren’t promising. Retroviruses are notoriously difficult to detect. The immune system doesn’t efficiently make antibodies against them and infections can persist at extremely low levels, but still cause symptoms like those in CFS. The XMRA theory made sense.
Yet the science quickly fell apart. Federal government agencies and European scientists got involved. Repeated failure to detect the virus prompted researchers to consider alternate explanations that effectively ended most worries about the virus.
The Death of a Theory
The debate reached its apex in 2010 when researchers found that XMRV came from a single prostate cancer cell line grown in lab dishes. All of the XMRV lab results isolated from patients came from a single lab-grown cancer cell line.
The implication was that XMRV came from the lab cell lines rather than patients. XMRV detection in CFS patients was an artifact, the product of hard-to-track-down contamination derived from a cell line that had picked up the laboratory virus during experiments with mice.
By 2012, the XMRV hypothesis was scientifically dead and buried. A study that cost taxpayers $2.3-million, funded by the U.S. National Institutes of Health (NIH), found no evidence to support XMRV to chronic fatigue syndrome.
W. Ian Lipkin, a molecular epidemiologist at Columbia University in New York, shepherded the effort. When things get tough in infectious viral disease, Lipkin is the guy they call. Between 2002 and 2010, his lab got 10,000 samples a year and discovered at least 400 new viruses. This scientist knows his stuff. He’s worked on West Nile Virus and a viral infection link to autism. But there were a few wrinkles in the XMRA studies: some people were infected with XMRV, even if it wasn’t associated with CFS.
The Cause May Be More Complicated
Scientists have put the XMRV hypothesis behind them. But, I’m not satisfied. How did a mouse virus get into people in the first place? Has an evolutionary super-virus developed in a lab escaped and gone global? Why do I find clusters of many viruses like EBV, CMV, HHV-6, HSV-2, and other infections like mycoplasma in my CFS patients’ labs? Why do I find deficiencies in their T-Lymphocyte counts? Why don’t they get better?
Like we’ve done for the last 30 years, doctors keep trying different therapies on CFS patients even though scientists haven’t yet nailed down a cause. But, is there one causative pathogen?
The whole saga of XMRV requires questioning the traditional medical paradigm that there is one cause for each disease. Viruses seem to play a role in CFS, but is one virus the specific cause?
In the mean time, I keep looking at the biomarkers in patient lab tests, testing innovative therapies, scouring the scientific literature, and attending the conferences in the hope of finding clues.
Discover Magazine: Chasing the Shadow Virus by Hillary Johnson, March 2013