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  • 5/19/2012

Interview with the World's Most Celebrated Virus Hunter: Ian Lipkin

part 3


So after all that, Borna does not cause any human disease at all?

I’ve seen no evidence of it, and we have not been able to demonstrate Borna virus infection in psychiatric patients or chronic fatigue syndrome patients. Having said that, we have recently shown that Borna virus sequences are integrated into the human genome and have been there for hundreds of thousands of years. Which means that at some point people have been infected with Borna virus. But whether they can currently be infected with it and whether it can be linked in a cause-and-effect relationship with disease are completely separate issues.


Your next big conquest involved a much more famous pathogen. You identified the West Nile virus after the first big U.S. outbreak in New York City in 1999. How did you get involved in that effort?

By August of 1999 I’m doing research in emerging diseases at the University of California, Irvine, and I’m invited to a meeting in Albany, New York, where we learned about an outbreak of what the Centers for Disease Control and Prevention [CDC] said was St. Louis encephalitis virus [SLE]. One investigator noted something unusual in people who had encephalitis that summer: Though otherwise healthy, they became especially weak and even required ventilators. Another noticed that crows were dying, along with a lot of animals in the Bronx Zoo. The CDC said, we don’t want to be bothered by these birds, and these other things are not relevant. We’re trying to address this SLE. But no one could isolate the agent. Then the CDC sent us the samples, and in 48 hours we knew that it was not SLE, and it was growing in the brain. We found material from the brain that matched the flavivirus family, to which West Nile belongs. Then we sequenced the genome. We were the first to clone an entire genome out of degraded human material. We reported West Nile virus in human spinal fluid and blood.


You moved your lab from Irvine to Columbia University in New York City around the time ofل ؟ 9/11. It must have been an extraordinary time for a pathogen hunter. There were the anthrax attacks and the global panic over severe acute respiratory syndrome, or SARS.

SARS was the first plague of the 21st century. In the winter of 2002 we began hearing chatter that there was a new respiratory disease in southern China. Most people thought it was probably some variant of flu, but then we found it was a coronavirus, so called because it’s spherical with a little crown [corona in Latin] composed of spikes of protein. It was a surprise because coronaviruses aren’t typically associated with human disease. We found we could grow the virus in certain cell types, and I began trying to develop a rapid molecular test, but it turned out not to be very sensitive. So we obtained some information about the virus’s genetic sequence and developed a real-time PCR assay [using a technique that rapidly replicates a stretch of DNA] that was 50 to 100 times more sensitive.

Chinese public health officials must have been interested in that.

The Chinese consulate invited me to a magnificent banquet at an East Side Chinese restaurant in New York. Halfway through the meal they said to me, we need you to go to Beijing tonight. People were dying there. It was the middle of an outbreak. And there was no treatment. I said, well, I can’t go by myself. So I convinced Thomas Briese, my colleague at Columbia, to come along. The morning we flew out, my kid is crying. Thomas’s wife is crying. I’m traveling with a suitcase filled with booties, gloves, masks, and 10,000 test kits for SARS. Nobody was going into Beijing because people were dying there. There were only three people on the final leg of the flight””Thomas, me, and Elisabeth Rosenthal from The New York Times. She was picking up her kid.


What happened when you arrived?

Chen Zhu, now China’s minister of health, was waiting at the airport with a red carpet. The streets were deserted. Tiananmen Square was empty. The Forbidden City was empty. The next morning we went to the Great Hall, and I’m told I am there to design their SARS program. There were 250 people waiting to hear what I wanted them to do.

Eventually they did manage to obliterate SARS in China.

SARS was contained not because of a drug or vaccine but because we identified people who were infected or at risk, and we isolated them. When I went back to see Chen Zhu, he was in a hospital with an unexplained liver problem. At the nursing station they didn’t even have soap. The first thing I did was sit down with him, and I said, you must do two things for me. There can be no spitting on the sidewalks because this spreads all these germs. And doctors and nurses coming to see you must wash their hands. By the time I left his room half an hour later, there was a prohibition against spitting on sidewalks and there was soap and water and paper towels in hospitals.


Your newest research looks at a particularly insidious set of chronic diseases that can result from infection in the womb. These diseases can produce lifelong psychiatric effects. How does that work?

The connection between prenatal infection and damage to the fetus has long been known. Exposure to syphilis, at its most extreme, results in stillbirth. Prenatal exposure to infections could result in microcephaly [a neurodevelopmental disorder in which the circumference of the head is smaller than normal]. But if the damage is more subtle, subtle changes in behavior can result. The child is still breathing, the child is walking, the locomotor function is not so abnormal that it’s incompatible with life in our culture. There was a time when these children would have died in utero, but now they survive, and you see some of these abnormalities come to the fore.


Have we reached the point where we can link specific infections to specific psychiatric disorders?

No, the connection is much more complex. When I worked with LCMV, it became clear that any sort of perturbation could damage the nervous system. Nerves find their way to specific locations through signposts that are part of the immune system. And if you increase immunological molecules of certain types, a nerve may jog this way as opposed to the way it’s supposed to go. It may not make a difference what the infectious agent is””bacterial, viral, or parasitic.

Source: discovermagazine.com

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