Byline: Dr. Jeffrey Taubenberger and Jared Lipworth
"Secrets of the Dead: Killer Flu" on PBS follows Jeffrey Taubenberger and his team of scientists seeking to learn where the 1918 flu virus came from and what made it so deadly. Using fragments of undamaged 1918 virus found in lung tissue of a flu victim, Taubenberger and his team set out to map the genes of the killer flu.
Since the original broadcast of this program, Taubenberger's team has created a genetic sequencing of the 1918 virus and has resurrected the virus itself to study its effects on lung tissue. This fall the team announced a striking similarity between the 1918 virus and today's H5N1 avian flu virus. Their findings indicate that the 1918 virus originated as a bird flu. The updated episode includes new material and interviews with Taubenberger that reflect these new findings. Secrets of the Dead: Killer Flu aired on PBS on Monday, Nov. 21, at 10 p.m. ET. (Check Local Listings.)
Taubenberger and executive producer Jared Lipworth were online Tuesday, Nov. 22, at noon ET to examine the 1918 flu virus and to discuss this episode of Secrets of the Dead.
Since 1994, Taubenberger has served as chief of the division of molecular pathology at the Armed Forces Institute of Pathology in Washington, D.C. He received his M.D. and Ph.D. degrees from the Medical College of Virginia and completed his residency in pathology at the National Cancer Institute. His clinical activities involve diagnostic molecular genetics. He holds dual board certifications in anatomic pathology and molecular genetic pathology from the American Board of Pathology and the American Board of Medical Genetics.
As executive producer for science programs, Lipworth is responsible for commissioning and overseeing all science programs produced by Thirteen/WNET New York. Current projects in production or development include "War Plane," "Secrets of the Dead V," "The Human Spark," "The Mysterious Human Heart" and "Big Ideas II." Prior to becoming executive producer, he was the series producer for the department's technology series, "Innovation." In 2003, Lipworth was nominated for a writing Emmy for "Secrets of the Dead: Mystery of the Black Death."
The transcript follows.
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Salt Lake City, Utah: Please address the evidence that suggests to you that the 1918 Spanish Flu was likely to have infected humans directly from the avian population, rather than involving an intermediate mammalian host. Thank you.
Dr. Jeffrey Taubenberger: There may well have been an intermediate host involved in the formation of the 1918 pandemic, we just don't know. If there was, we don't know what species. Molecular evidence fits the historical picture that humans gave the virus to pigs, not the other way around; so it probably wasn't pigs. What we think is different about the 1918 pandemic compared to the 1957 or 1968 pandemics is that it doesn't look like a mixed or "reassorted" human-bird virus, but an entirely bird-like virus that adapted to humans.
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Charleston, W.Va.: Right now the H5N1 seems particularly virulent with a mortality rate between 33-50 percent. I have seen in print articles that, based on history, the virulence decreases as the virus causes a pandemic. Is that always the case? Would the decrease be due to a genetic mutation or recombination? It is hard to sort through all of the information available. Thanks!
Dr. Jeffrey Taubenberger: It is likely that virulence would decrease if a new virus, like H5N1 adapted to become transmissible to humans, although we cannot predict with certainty what will happen with any given pathogen. But in general, pathogens that kill a large percentage of victims quickly are thought to spread less well (for example Ebola) than those that can be spread by people who are not debilitated. These changes would undoubtedly be due to mutations in the viral genome. At this time we do not know which mutations are critical to allow an animal-adapted virus to become transmissible in humans. We know that the 1918 virus was very transmissible, and that the current H5N1 viruses are very poorly transmissible in humans. so, differences in their genomes are likely to be important in working out this process.
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Jared Lipworth: Hi everyone. Thanks so much for watching last night's Secrets of the Dead program and for joining us today in the chat. And a special thanks to Dr. Taubenberger for making himself available--I can only imagine how busy his schedule is these days...
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Arlington, Va.: Jared, when and why did you decide to update this film? Due to recent news/concerns expressed about the flu - or before that? Thank you.
Jared Lipworth: Really, as soon as we heard that Dr. Taubenberger had finished sequencing the 1918 genome we knew we had to update the film. When it originally aired, he was still working on it, and now we had the chance to see the sequence completed and to see firsthand what he had learned. The fact that Dr. Taubenberger could talk about the similarities and differences between the 1918 virus and today's avian strains made it even more relevant. Secrets of the Dead is always looking to make important connections between past events and our world today, so this was an excellent and important opportunity to do so.
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Arlington, Va.: Dr., what did you learn overall about mutation of viruses during your research? Applying what you've learned to what's going on today, do you think the avian flu will mutate? Thank you.
Dr. Jeffrey Taubenberger: We are trying to understand two basic things about the 1918 influenza - how did the pandemic virus form?, and why was it so virulent? Having the complete sequence is helping us to answer these questions. But even more importantly we are trying to understand the lessons of the 1918 virus to learn more general rules about how pandemics form and cause disease. for example we have found that the H5N1 viruses share some changes with 1918 that we think will be important for the virus adapting to humans. Whether the H5N1 virus will ultimately acquire the ability to become human adapted is an open question. Obviously we hope not, but we need to be vigilant about monitoring the virus for these kinds of changes.
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Vienna, Va.: I wasn't surprised at the discovery that the 1918 flu virus acted by creating a cytokine storm. The very symptoms (black feet and so on) was very similar to Ebola and hantaviruses, which also kill mostly due to the immune system's own overreaction. I'm in one of the few families that have a written history of those times, so I grew up knowing about the 1918 flu. I was amazed that so many of my generation had never heard of it... at least until a few years ago when the 1918 flu became a hot topic.
That said, what is the major age group that the current H5N1 virus is infecting and killing?
Dr. Jeffrey Taubenberger: We don't really know yet what made the 1918 virus virulent. The animal models do suggest a very robust immune response which may indeed have contributed to the progression of disease. Remember however that individual responses to the identical virus can very tremendously. Even in 1918, about a third of those exposed developed no symptoms, and of those made ill, the vast majority recovered. Case mortality rate in the U.S. was around 2.5%. What we need to figure out still is whether people of the young adult age group had this unusual "over-robust" immune response or another kind of unusual immune reaction to the virus relating to their previous exposure history to flu viruses. Unfortunately we do not yet know anything about the human influenza viruses that circulated before 1918.
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Ventura, Calif.: Temperature at which the virus thrives appears very important. As long as it remains high, avian, the disease appears to lodge in the lungs. Question, you envision the virus becoming more mammalian, thriving at cooler temperature, and thus lodging higher up the respiratory tract, and thusly more easily transmitted, ie, pandemic. How will this occur?
Dr. Jeffrey Taubenberger: Yes, the optimal temperature for viral replication is likely to be important for switching hosts. There are several mutations in the polymerase genes (encoding the proteins that copy the viral genetic material)that might be important because they change the temperature optimum of the polymerase complex. The genetic details of what needs to take place for a bird virus to adapt to a mammalian host are just not yet clear.
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Chicago, Ill.: When do you think we will have a vaccination for H5N1?
