The Scientist: 'The “Virus Hunter” Who Advanced Public Health, One Tool at a Time'
In his 40-year epidemiology career, Ian Lipkin has done it all: from discovering 2,000 viruses to solving a nationwide SARS crisis.
by Shelby Bradford, PhD
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'Alongside his pathogen discovery work at the turn of the 21st century, Lipkin became interested in gene-environment-timing interactions influencing autism spectrum disorder (ASD), in part because a relative had the condition. When he moved to Columbia University he was introduced to Camilla Stoltenberg, an epidemiologist at the Norwegian Institute of Public Health. She described a newly organized study, the Norwegian Mother and Child Cohort, that could provide a source of unbiased samples to explore ASD risks.
Lipkin jumped at the opportunity to explore environmental interactions associated with autism. This led to the creation of the Autism Birth Cohort. While the study is ongoing, data has pointed to a strong relationship between fever during pregnancy and autism risk.'
At the same time, Lipkin began applying the techniques he developed studying Bornavirus to cases of undiagnosed encephalitis and central nervous system infections.20,21 This led him to the field of the poorly understood condition of myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS).
[Avindra] Nath, who was also studying these disorders, explained that one of the difficult elements of studying ME/CFS and unexplained encephalitis has been that the symptoms are subjective and, until recently, many doctors dismissed these patients or attributed the symptoms to psychological causes. “Nobody knows what’s wrong with [these patients],” he said. “[Doctors] keep treating them with all kinds of things, and sometimes they get better, and oftentimes, they don’t. They even get worse.”
Nath and Lipkin began their ME/CFS studies independently with their own cohorts, but shared samples and advice with one another. “What is remarkable about it is that I think both of us, independently, came to the same conclusion,” Nath said. “There is a unique immune dysfunction in these patients, and it could very well be driven by the infectious process that they never got rid of completely.”
Lipkin described the challenge in advancing the understanding of these disorders. “You not only need to be able to detect the agents itself, but you need to be able to detect footprints, and those footprints are immune responses.” His group identified that patients with ME/CFS display sustained levels of cytokines, often following an infection, and provided evidence that these patients may also have dysfunctional peroxisomes.'
In his 40-year epidemiology career, Ian Lipkin has done it all: from discovering 2,000 viruses to solving a nationwide SARS crisis.
by Shelby Bradford, PhD
----
'Alongside his pathogen discovery work at the turn of the 21st century, Lipkin became interested in gene-environment-timing interactions influencing autism spectrum disorder (ASD), in part because a relative had the condition. When he moved to Columbia University he was introduced to Camilla Stoltenberg, an epidemiologist at the Norwegian Institute of Public Health. She described a newly organized study, the Norwegian Mother and Child Cohort, that could provide a source of unbiased samples to explore ASD risks.
Lipkin jumped at the opportunity to explore environmental interactions associated with autism. This led to the creation of the Autism Birth Cohort. While the study is ongoing, data has pointed to a strong relationship between fever during pregnancy and autism risk.'
At the same time, Lipkin began applying the techniques he developed studying Bornavirus to cases of undiagnosed encephalitis and central nervous system infections.20,21 This led him to the field of the poorly understood condition of myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS).
[Avindra] Nath, who was also studying these disorders, explained that one of the difficult elements of studying ME/CFS and unexplained encephalitis has been that the symptoms are subjective and, until recently, many doctors dismissed these patients or attributed the symptoms to psychological causes. “Nobody knows what’s wrong with [these patients],” he said. “[Doctors] keep treating them with all kinds of things, and sometimes they get better, and oftentimes, they don’t. They even get worse.”
Nath and Lipkin began their ME/CFS studies independently with their own cohorts, but shared samples and advice with one another. “What is remarkable about it is that I think both of us, independently, came to the same conclusion,” Nath said. “There is a unique immune dysfunction in these patients, and it could very well be driven by the infectious process that they never got rid of completely.”
Lipkin described the challenge in advancing the understanding of these disorders. “You not only need to be able to detect the agents itself, but you need to be able to detect footprints, and those footprints are immune responses.” His group identified that patients with ME/CFS display sustained levels of cytokines, often following an infection, and provided evidence that these patients may also have dysfunctional peroxisomes.'