Wow! This is awesome! It really does say something about symbiosis vs pathogens. Very interesting. It makes sense that it is part genetic and part trigger, especially in view of twins.This part explains a lot:
In 1970 Torrey arrived at the National Institute of Mental Health in Washington, D.C., having finished his training in psychiatric medicine. At the time, psychiatry remained under the thrall of Freudian psychoanalysis, an approach that offered little to people like Rhoda. Torrey began looking for research opportunities in schizophrenia. The more he learned, the more his views diverged from those of mainstream psychiatry.
A simple neurological exam showed Torrey that schizophrenics suffered from more than just mental disturbances. They often had trouble doing standard inebriation tests, like walking a straight line heel to toe. If Torrey simultaneously touched their face and hand while their eyes were closed, they often did not register being touched in two places. Schizophrenics also showed signs of inflammation in their infection-fighting white blood cells. 'If you look at the blood of people with schizophrenia,' Torrey says, 'there are too many odd-looking lymphocytes, the kind that you find in mononucleosis.' And when he performed CAT scans on pairs of identical twins with and without the disease—including Steven and David Elmore—he saw that schizophrenics' brains had less tissue and larger fluid-filled ventricles.
Subsequent studies confirmed those oddities. Many schizophrenics show chronic inflammation and lose brain tissue over time, and these changes correlate with the severity of their symptoms. These things 'convinced me that this is a brain disease,' Torrey says, 'not a psychological problem.'
By the 1980s he began working with Robert Yolken, an infectious-diseases specialist at Johns Hopkins University in Baltimore, to search for a pathogen that could account for these symptoms. The two researchers found that schizophrenics often carried antibodies for toxoplasma, a parasite spread by house cats; Epstein-Barr virus, which causes mononucleosis; and cytomegalovirus. These people had clearly been exposed to those infectious agents at some point, but Torrey and Yolken never found the pathogens themselves in the patients' bodies. The infection always seemed to have happened years before.
Torrey wondered if the moment of infection might in fact have occurred during early childhood. If schizophrenia was sparked by a disease that was more common during winter and early spring, that could explain the birth-month effect. 'The psychiatrists thought I was psychotic myself,' Torrey says. 'Some of them still do.'
Better prenatal care or vaccinations could prevent the infections that put people on a path to schizophrenia, and early treatment might prevent psychosis from developing two decades later.While Torrey and Yolken were chasing their theory, another scientist unwittingly entered the fray. Hervé Perron, then a graduate student at Grenoble University in France, dropped his Ph.D. project in 1987 to pursue something more challenging and controversial: He wanted to learn if new ideas about retroviruses—a type of virus that converts RNA into DNA—could be relevant to multiple sclerosis.
Robert Gallo, the director of the Institute of Human Virology at the University of Maryland School of Medicine and co*discoverer of HIV, had speculated that a virus might trigger the paralytic brain lesions in MS. People had already looked at the herpes virus (HHV-6), cytomegalovirus, Epstein-Barr virus, and the retroviruses HTLV-1 and HTLV-2 as possible causes of the disease. But they always came up empty-handed.
Perron learned from their failures. 'I decided that I should not have an a priori idea of what I would find,' he says. Rather than looking for one virus, as others had done, he tried to detect any retrovirus, whether or not it was known to science. He extracted fluids from the spinal columns of MS patients and tested for an enzyme, called reverse transcriptase, that is carried by all retroviruses. Sure enough, Perron saw faint traces of retroviral activity. 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 moved to the National Center for Scientific Research in Lyon, France, where he labored days, nights, and weekends. 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.
After eight years of research, Perron finally completed his retrovirus's gene sequence. What he found on that day in 1997 no one could have predicted; it instantly explained why so many others had failed before him. We imagine viruses as mariners, sailing from person to person across oceans of saliva, snot, or semen—but Perron's bug was a homebody. It lives permanently in the human body at the very deepest level: inside our DNA. After years slaving away in a biohazard lab, Perron realized that everyone already carried the virus that causes multiple sclerosis.
Other scientists had previously glimpsed Perron's retrovirus without fully grasping its significance. In the 1970s 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. So began a strange chapter in evolutionary biology.
