• News

Study examines origins of Spanish flu outbreak

By Amina Khan, Los Angeles Times September 23, 2011, 5:47 p.m. In 1918, the virus circulated for months before the deadly epidemic was identified. The study offers potential lessons to deal with a modern outbreak. The film “Contagion” may have been fiction, but the 1918-19 influenza epidemic was horrifyingly real. The “Spanish flu” epidemic tore a path of destruction across the globe, killing an estimated 50-100 million people within months before disappearing into history. Now, evidence from U.S. soldiers felled by the virus reveals that it circulated in the country for four months before the pandemic was even identified. The findings, published online Monday in the journal Proceedings of the National Academy of Sciences, offer a picture of a virus as it turned from common pathogen to killer bug, said senior author Jeffery Taubenberger, a pathologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Md. “This was one of the worst infectious disease outbreaks that ever occurred,” Taubenberger said. And without examining samples of the virus and infected tissues, he added, “there’s no way to understand what happened here.” The Spanish flu was officially identified in September 1918, but Taubenberger’s team suspected it may have been circulating within people earlier than that. To get at the question, they examined lung tissue, preserved in formaldehyde and stuck in paraffin wax, from 68 U.S. soldiers who died in training camps between March 1, 1918 and Feb. 28, 1919. The scientists found signs of the virus, including pieces of its genetic material, showing that several soldiers had contracted the bug well before the pandemic took off. Damage and inflammation to the tissue samples also matched what the researchers expected to see from an influenza infection. Analysis of the genetic material also showed that at that point, the virus was still adapted to attach itself to certain cell receptors in birds, its natural hosts, and not as effectively to those in the respiratory tract of human beings. But the virus that emerged a few months later was far better targeted toward the human respiratory tract — making it dangerously effective. Still, this still doesn’t explain what other factors allowed the virus to spread from human to human so quickly, said Robert Webster, a virologist at St. Jude Children’s Research Hospital in Memphis, Tenn., who was not involved in the study. Understanding the way the 1918 virus functioned, changed and spread could help researchers develop better strategies and treatment to fight the pandemic flu threats of today — including, perhaps, the closely-held dream of a universal influenza vaccine, he said. The findings already have yielded some lessons. All 68 cases showed evidence of bacterial pneumonia as well as virus infection — suggesting that secondary bacterial infections contributed to the carnage and that doctors should keep antibiotics handy when dealing with influenza patients. “This one-two punch is particularly important for public health officials to be aware of,” Taubenberger said. Should the Spanish flu virus infect us today, it would do “nothing. Little or nothing,” Webster said. After pandemics, the responsible viruses still circulate but are defanged because our immune systems now know them. The 2009 H1N1 flu, Webster noted, “is its grandchild.” http://www.latimes.com/news/science/la-sci-spanish-flu-20110924,0,7980470.story