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Soon he obtained fuzzy electron microscope images of the retrovirus itself. His discovery was intriguing but far from conclusive. After confirming his find was not a fluke, Perron needed to sequence its genes. He cultured countless cells from people with MS to grow enough of his mystery virus for sequencing. MS is an incurable disease, so Perron had to do his research in a Level 3 biohazard lab. Working in this airtight catacomb, he lived his life in masks, gloves, and disposable scrubs.

What he found on that day in no one could have predicted; it instantly explained why so many others had failed before him. It lives permanently in the human body at the very deepest level: inside our DNA.

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After years slaving away in a biohazard lab, Perron realized that everyone already carried the virus that causes multiple sclerosis. In the s biologists studying pregnant baboons were shocked as they looked at electron microscope images of the placenta. They saw spherical retroviruses oozing from the cells of seemingly healthy animals. They soon found the virus in healthy humans, too.

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So began a strange chapter in evolutionary biology. Viruses like influenza or measles kill cells when they infect them. Sixty million years ago, a lemurlike animal—an early ancestor of humans and monkeys—contracted an infection. When the lemur reproduced, that retrovirus rode into the next generation aboard the lucky sperm and then moved on from generation to generation, nestled in the DNA. But such genetic intrusions stick around a very long time, so humans are chockablock full of these embedded, or endogenous, retroviruses.

If our DNA were an airplane carry-on bag and essentially it is , it would be bursting at the seams. Our body works hard to silence its viral stowaways by tying up those stretches of DNA in tight stacks of proteins, but sometimes they slip out. Now and then endogenous retroviruses switch on and start manufacturing proteins.

They assemble themselves like Lego blocks into bulbous retroviral particles, which ooze from the cells producing them. Endogenous retroviruses were long considered genetic fossils, incapable of doing anything interesting. By the time Perron made his discovery, Torrey and Yolken had spent about 15 years looking for a pathogen that causes schizophrenia. They found lots of antibodies but never the bug itself.

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The team wondered if other retroviruses might cause these symptoms in separate diseases such as schizophrenia. In they nabbed a possible culprit. Several other studies have since found similar active elements of HERV-W in the blood or brain fluids of people with schizophrenia. Much of their research revolves around the contents of a nondescript brick building near Washington, D. Inside are hundreds of cadaver brains donated to science by the deceased , numbered 1 through Each brain is split into right and left hemispheres, one half frozen at about — degrees Fahrenheit, the other chilled in formaldehyde.

Jacuzzi-size freezers fill the rooms. New high-speed DNA sequencing is making the job possible. Fixed to that plate are million magnetic beads, and attached to each bead is a single molecule of DNA, which the machine is sequencing. In a week the machine churns out the equivalent of six human genomes—enough raw data to fill 40 computer hard drives. RNA is a messenger of DNA, a step in the path to making proteins, so its presence could mean that viral proteins are being manufactured in the body more frequently than had been thought.

Although the body works hard to keep its ERVs under tight control, infections around the time of birth destabilize this tense standoff. White blood cells vomit forth inflammatory molecules called cytokines, attracting more immune cells like riot police to a prison break. The scene turns toxic.

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The mice became clumsy, then paralyzed, then died of brain hemorrhages. It was an extreme experiment, but to Perron it made an important point. In MS the immune system directly attacks and kills brain cells, causing paralysis. In schizophrenia it may be that inflammation damages neurons indirectly by overstimulating them. The first, pivotal infection by toxoplasmosis or influenza and subsequent flaring up of HERV-W might happen shortly before or after birth. That would explain the birth-month effect: Flu infections happen more often in winter.

The initial infection could then set off a lifelong pattern in which later infections reawaken HERV-W, causing more inflammation and eventually symptoms. This process explains why schizophrenics gradually lose brain tissue. It explains why the disease waxes and wanes like a chronic infection.

And it could explain why some schizophrenics suffer their first psychosis after a mysterious, monolike illness. The infection theory could also explain what little we know of the genetics of schizophrenia. One might expect that the disease would be associated with genes controlling our synapses or neurotransmitters.

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Gene studies have failed to provide simple explanations for ailments like schizophrenia and MS. Genes may come into play only in conjunction with certain environmental kicks. Retroviruses, including HIV, are known to be awakened by inflammation—possibly the result of infection, cigarette smoke, or pollutants in drinking water. The era of writing off endogenous retroviruses and other seemingly inert parts of the genome as genetic fossils is drawing to an end, Perron says.

Schizophrenia treatments were limited when she fell ill. Early on she received electroshock therapy and insulin shock therapy, in which doctors induced a coma by lowering her blood sugar level. Rhoda Torrey has spent 40 years in state hospitals. The disease has left only one part of her untouched: Her memory of her brief life before becoming ill—of school dances and sleepovers half a century ago—remains as clear as ever.

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Steven Elmore was more fortunate. Drug therapy was widely available when he fell ill, and although he still hears voices from time to time, he has done well. Now 50 years old, he is married, cares for an adopted son and stepson, and works full time. He has avoided common drug side effects like diabetes, although his medications initially caused him to gain 40 pounds. Torrey and Yolken hope to add a new, more hopeful chapter to this story.

Looking ahead, better prenatal care or vaccinations could prevent the first, early infections that put some people on a path to schizophrenia. For high-risk babies who do get sick, early treatment might prevent psychosis from developing two decades later. The company has created an antibody that neutralizes a primary viral protein, and it works in lab mice with MS. A clinical trial with schizophrenics might follow in Even after all that, many medical experts still question how much human disease can be traced to viral invasions that took place millions of years ago.

If the upcoming human trials work as well as the animal experiments, the questions may be silenced—and so may the voices of schizophrenia. Other Scientists are Concerned.


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The Sciences. Planet Earth. Mind The Insanity Virus Schizophrenia has long been blamed on bad genes or even bad parents. Wrong, says a growing group of psychiatrists. Newsletter Sign up for our email newsletter for the latest science news. Sign Up. Rhoda Torrey and her brother Fuller, who would go on to research shizophrenia.