Spanish flu link could explain H1N1's spread

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It seemed to come out of nowhere in April, when it was diagnosed in two unrelated children in California. But evidence from different studies appears to tie the novel influenza A H1N1 to the family of the 1918 Spanish flu virus, one of the deadliest of the modern era and blamed for the deaths of 20 million to 50 million people.


However, the new strain lacks a key genetic component of that virus that made it so lethal, and novel H1N1 appears to be so far no worse and possibly milder than normal seasonal flu, experts said. The tie to that older virus, however, could help explain why the new virus seems to be infecting younger people more and sparing the elderly.

Using blood samples collected as part of clinical trials and other means dating as far back as 1880, Jackie Katz of the Centers for Disease Control and Prevention and colleagues looked for antibody reactions to novel H1N1. Their study was published this month in the New England Journal of Medicine .

"In individuals born after 1980, there's very low levels of cross-reactive antibody to novel H1N1 virus," Dr. Katz said at a flu conference at the University of Georgia this past summer. "But as we go backwards and increase in age, it peaks around the time when individuals may have experienced a 1918-like virus."

Their study found that only 4 percent of those born after 1980 had moderate levels of cross-reactive antibodies while 34 percent born before 1950 had higher levels of those antibodies. There seemed to be no benefit of recent seasonal influenza vaccination in that younger population but there did in those who might have previously been exposed to an older virus and who received the 1976 swine flu vaccine, which the study notes was about 45 million people or 20 percent of the U.S. population. More than half of the blood samples from people who were 25 and older when they received the 1976 vaccination showed evidence of cross-reaction to the 2009 novel H1N1 virus, the study notes.

These findings could help explain the current distribution of flu cases, Dr. Katz said, which eschews the normal course of seasonal flu in striking the elderly population more.

"There is some level of cross-reactive antibody in older individuals to (novel) H1N1 and it may well play a role in the epidemiology" of the pandemic, she said. About 79 percent of confirmed cases were in people age 30 or younger while only 2 percent were in people 60 and older, the study notes.

There might be even more direct evidence of a tie to a Spanish-flu-type virus. Flu viruses can sometimes jump from pigs and birds to people and vice versa. The 2009 novel H1N1 is a triple reassortment swine flu and contains human, swine and avian parts, said Ralph Tripp, the associate director of the Influenza Pathogenesis and Immunology Research Center, a joint center of excellence in influenza between the University of Georgia and Emory University. It appears to have been circulating in North American pig herds since the 1990s.

"In this particular virus, the H (hemagglutinin) gene was derived from the 1918 swine virus," he said. But that particular gene is not what made the 1918 virus so deadly, Dr. Tripp said. It was a mutation known as PB1-F2 that allows the virus to replicate more quickly inside the host cell.

Scientists at the UGA-Emory lab are helping to conduct surveillance of the novel H1N1 virus, one of six regional centers of excellence funded by the National Institutes of Health.

So far, there is no evidence the current novel virus has acquired the mutation that would allow it to become more virulent, Dr. Tripp said. In fact, clinicians are reporting that in most patients the virus does not appear to be any worse and could possibly be milder than seasonal flu.

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Augusta not spared from spanish Flu

Anything that draws comparisons to the 1918 Spanish flu epidemic gets the attention of those in public health, and with good reason. The outbreak from 1918-1919 is thought to have killed as many as 21 million worldwide and some estimates go up to 50 million.

In his book The Great Influenza, author John M. Barry claims it is the deadliest disease outbreak in human history, worse than the plagues of the 1300s.

"Influenza killed more people in a year than the Black Death of the Middle Ages killed in a century; it killed more people in 24 weeks than AIDS has killed in 24 years," Mr. Barry wrote. And it killed many young healthy adults, unlike regular flu that hits the very young and the elderly the hardest.

Augusta was not spared in that pandemic, according to Mr. Barry's book.

A train carrying 3,108 troops from Camp Grant in Illinois left in September 1918 for a 950-mile journey to Camp Hancock, outside Augusta, according to the book.

Camp Grant had seen an outbreak just days before and by the time the cramped train arrived, many of those on board were severely ill.

Seven hundred were taken immediately to the camp's hospital and 2,000 from that trip would eventually be hospitalized from influenza, with 143 deaths according to the book.

By October, there were 3,000 hospitalized at the camp and 52 died in a single week, according to The Story of Augusta by Edward J. Cashin.

"The Board of Health quarantined the Camp and closed all schools, churches and theaters in Augusta until the worst was over in late November," Mr. Cashin wrote.

Like the current novel H1N1, the 1918 virus seemed to appear out of nowhere in the spring in a milder form and then turned deadlier in the fall. But there the comparison stops because the current virus has not turned more virulent and in fact lacks the mutations that made the 1918 virus so lethal.