Two years into her illness, Erin was broken. On any given day, she would cycle through a laundry list of symptoms: brain fog, dizziness, light sensitivity, a sore throat, nausea, swollen lymph nodes, crushing fatigue, a racing heart, ear ringing, drenching sweats and fainting.

During this time, she had lost some of her most active and athletic friends, who grew impatient with the waxing and waning symptoms that prevented her from the leaving the house on most days.

“I had times where I’d shut the blinds, lie down and hope for a better day,” says Erin. “Literally, my escape was through my dreams. I just couldn’t stand to be in my body.”

Her life revolved around doctors’ appointments. One physician ruled out infectious diseases. Neurologists examined her for seizure disorders and brain tumors. A rheumatologist evaluated her for systemic lupus erythematosus and other inflammatory diseases. An endocrinologist agreed that the origin of her fatigue was not the thyroid, the adrenals or any other gland. A cardiologist assured her it was not her heart.

None of them could settle on a definitive diagnosis, so the physicians tagged her with the insurance code for chronic fatigue syndrome, a controversial diagnosis for a set of symptoms also sometimes labeled as CFIDS — for chronic fatigue and immune dysfunction syndrome — and ME — for myalgic encephalomyelitis. The dominant moniker today is ME/CFS.

No one knows what causes ME/CFS. Some think that an infectious agent or overactive immune system triggers it. Others blame genetic flaws, environmental factors or a combination of any of the above.

Roughly 17 million people worldwide (1 million to 4 million in the United States) have ME/CFS. It strikes people of all ages and racial, ethnic and socioeconomic groups. It is diagnosed two to four times more often in women than men.

It’s a syndrome that gets little respect in the medical community because, with no tangible cause and an ever-changing constellation of symptoms, patients often get labeled as hypochondriacs, malingerers or seekers of addictive pain medications. The primary diagnostic criterion for this condition is infuriatingly vague — “six or more consecutive months of severe fatigue” — virtually unchanged since 1994.

As Erin went from specialist to specialist, well-meaning doctors grew frustrated with their inability to help her. One day Erin blacked out while driving, almost hitting a streetlight. After another fainting accident, an emergency room physician told her, “On hot days, women faint.”

“I felt objectified, like a slab of meat,” says Erin.

Finally, in 2009 Erin was diagnosed with postural orthostatic tachycardia syndrome — which accounted for her fainting spells. For treatment, her cardiologist sent her to Stanford Hospital’s cardiology clinic to see one of the nation’s few POTS specialists, cardiac electrophysiologist Karen Friday, MD.

POTS, which often accompanies ME/CFS, is a fainting disorder associated with an abnormal increase in heart rate and low blood pressure. The mechanism is unknown, but some people develop it after contracting viral or bacterial infections like mononucleosis, pneumonia or Lyme disease. Friday prescribed fludrocortisone to manage Erin’s low blood pressure, but to explore the possibility of an underlying microbial trigger, she sent Erin to see Stanford professor of infectious diseases José Montoya, MD.

Montoya, 54, dapper in his white coat and tie and smiling widely, greeted Erin with a bear hug and told her in his thick Colombian accent, “I want to make your life beautiful again.”

“Dr. Montoya was a shining beacon of hope,” says Erin.

Montoya’s ethos to reduce patient suffering was shaped by a hardworking, single mother and the iron-fisted priests at his Catholic school in Cali, Colombia. He was accepted into medical school at age 18, after receiving the third-highest qualifying exam score in his native country that year. After medical school he went on to Tulane University School of Medicine for his residency, then joined the infectious disease division at Stanford. At Stanford he became a world-recognized authority on infections affecting heart transplant recipients and on toxoplasmosis, a common parasitic disease.

Montoya conducted a detailed medical history and physical exam on Erin, then ordered a battery of tests for viruses, bacteria and fungi. His wide-net diagnostic approach paid off; he found two blood-borne microbes — Human Herpesvirus-4 and the coxsackie virus — known to cause chronic disease and POTS.

Though Montoya wasn’t sure if these viruses were at the root of Erin’s illness or merely collateral infections, he started her on a high dose of the antiviral drug famciclovir. Erin was relieved to finally have a physician who wasn’t going to punt her case to another specialist.

“I wanted to live my life again,” says Erin.

Montoya is one of only a handful of clinician-researchers who accept ME/CFS patients, and he currently has a waiting list of about 150.

Back in 2005, while attending a conference on toxoplasmosis in Paris, Montoya told his mentor that he wanted to research ME/CFS. His mentor scoffed at the idea, pointing to a homeless person lying in a Parisian gutter.

“That’s going to be you if you go into chronic fatigue research,” the mentor told him.

The hard truth is that most medical research labs rely in large part on U.S. government funding, and the ME/CFS research budget is insufficient to support a typical university research lab.

The National Institutes of Health, the largest funder of medical research in the United States, allocated only $5 million for ME/CFS research in 2013. (To put this in context, the annual NIH research budget for multiple sclerosis, with 400,000 sufferers, is $112 million.) The reasons behind this underfunding are complicated.

One factor is that the NIH funding process favors well-defined diseases that fit neatly into medical specialties like cardiology, cancer and neurology. Most of these medical societies have organized lobbying efforts, sometimes backed by pharmaceutical or medical technology companies. Another factor is that collectively ME/CFS patients are too sick to organize, raise money and lobby for research dollars. And then there is the stigma associated with the condition; some NIH grant reviewers are reluctant to fund research because they believe that ME/CFS is a psychosomatic, “all in the head,” disorder. (To remedy this, the NIH recently created a special emphasis panel so that researchers familiar with the condition review grant applications.)

But none of this deterred Montoya, who was driven to do something for the suffering patients queuing up for appointments.

Opportunity knocked in 2008 when a wealthy donor met with Montoya to talk about the ME/CFS problem. He asked if a $5 million donation for research could make a difference.

Montoya could hardly believe the sum, replying, “Yes, give me five years.”

With the freedom of private funding, Montoya was able to take a multifaceted and rigorous approach to analyzing ME/CFS. Traditionally, NIH funding is awarded through medical specialty groups that tend to favor research that tests one narrow hypothesis about a disease. For example, a researcher might get funded to screen blood samples for one virus, or treat patients with one drug. This approach takes a long time, and researchers typically aren’t able to share and build on discoveries for years.

Montoya’s game plan was to use a big-picture, big-data strategy to find out what was wrong with patients like Erin. His first step in launching the Stanford Initiative on Infection-Associated Chronic Diseases was to convince a dozen or so academic investigators to venture out of their comfort zones to research a wildly unpopular disease using technologies yet to be developed.

Montoya convinced experts in immunology, rheumatology, genetics, bioengineering, anesthesiology, neuroradiology, cardiology, psychiatry, infectious diseases and bioinformatics to all work together. The team members would be searching blood samples for infectious microbes, inflammation-related molecules and genetic flaws. They’d do brain scans and physical exams. They’d survey study subjects for fatigue levels and medical histories. Then they’d compare all this data with that of healthy people to see what was different. Next, he launched a Bay Area recruitment campaign for 200 patients who met the Centers for Disease Control’s definition for chronic fatigue syndrome, including Erin, and 400 age- and sex-matched healthy volunteers, all of whom agreed to donate eight tubes of blood and be poked, scanned and surveyed over the next decade.

The most complex part of the ME/CFS initiative was the exploration into what was happening with the immune system of these patients. For this role, he needed an expert who didn’t care about the ME/CFS stigma or how things have been done in the past. So he called on Mark Davis.

There will be blood

Davis, in well-worn jeans and running shoes, leans back in his chair, surrounded by pillar-piles of scientific papers. At first glance one might assume that he is — in California-speak — a mellow dude.

But looks can be deceiving, because Davis, who discovered how T cells help a body fight off infections, is all about the fight.

As if to prove this point, Davis reaches into a random stack of paper and pulls out a black-and-white photo of a collegiate fencing match.

“This is me,” he says, pointing to a man in white flying off the ground, plunging the tip of a silver foil directly between the eyes of a masked opponent. “I like to poke people.”

He then reaches into another stack of paper and pulls out the Dec. 19, 2008, issue of Immunity. It is a poke-in-the-eye to fellow immunologists, an essay titled, “A Prescription for Human Immunology.”

In this oft-quoted paper, he describes immunology as a field known for its “impenetrable jargon, byzantine complexity and acrimonious disputes.”

He also chides many of his colleagues for spending too much time on mouse studies and not enough on human studies. For immunological studies, mice are fast and easy. They can be bred with specific diseases, such as diabetes or Parkinson’s, and then dissected to evaluate the effectiveness of experimental treatments. There are relatively few regulatory, financial and ethical hurdles to working with mice. He emphasizes that lab mice live in isolated, disease-free, temperature-controlled environments, far different from the crowded, germ-ridden urban habitats of your typical Homo sapiens. (Most humans are infected with six different herpes viruses, and who knows what else.) The other problem with “mouse models” is that their common ancestors are genetically separated from Homo sapiens by some 65 million years.