# 321
For years there has been extensive debate over why the 1918 Spanish Flu was so very lethal. The last century saw 3 influenza pandemics; 1918, 1957, and 1968, with the fatalities seen in the first pandemic of the 20th century many times greater than the other two combined.
The demographics of the deaths in 1918 were startlingly different from what we normally see in an influenza outbreak, with a greater number of deaths seen among young healthy adults.
The dominant theory has been that the body’s immune system, when faced with a novel influenza virus, one that is genetically different from any it had seen before, goes into overdrive and inadvertently kills the host in its attempt to rid itself of the virus. This hyper-immune response is known as the `cytokine storm’.
Until now, all of this was pretty much theory; one that we had no way of independently testing. Scientists working in Canada in a Level 4 biosecurity containment laboratory have resurrected the 1918 virus (no easy feat), and have infected 7 macaques monkeys, and observed their response.
In this excellent article from the Canadian Press, Helen Branswell explains:
1918 flu virus, recreated in Winnipeg, triggered overwhelming immune response
HELEN BRANSWELL
(CP) - The virus that caused the 1918 influenza pandemic triggered an overwhelming immune response that swamped the lungs of macaque monkeys - the first primates deliberately infected with the Spanish flu virus, Canadian and American scientists reported Wednesday.
The research, done in part at the Public Health Agency of Canada's National Microbiology Laboratory in Winnipeg, supports the notion that the virulent flu virus turned the body's immune system against itself. Scientists believe that theory explains how the devastating influenza strain managed to mow down unprecedented numbers of healthy people in the prime of life.
Previous work, done by some of the same scientists, showed mice infected with the virus also experienced this hyper immune response, a so-called cytokine storm. (Cytokines are one of the proteins the immune system makes to fight infection.)
"There was an uncontrolled or aberrant inflammatory response," one of the authors, Dr. Michael Katze of the University of Washington in Seattle, explained in a telephone briefing.
"One possibility (is) . . . instead of protecting the individuals that were infected with the highly pathogenic virus, the immune response is actually contributing to the lethality of the virus."
Read the rest of Ms. Branswell’s article here.
The H5N1 virus, like the 1918 H1N1 virus that caused the Spanish flu, is a novel influenza virus, previously unseen in man. And much like in 1918, this bird flu (a misnomer, as all flu’s are avian in origin) of today, is many times more virulent than a normal flu.
To date, the reported death rate of the avian flu has exceeded 60%, which is far higher than anything reported in 1918. The demographic patterns are similar, with most infections, and deaths, reported in those between the ages of 10 and 40.
If the next pandemic should spring from the H5N1 virus (still an `if’), then children and young adults could be particularly at risk, as their immune systems are the strongest, and are most likely to evoke a cytokine storm response.
Today’s research helps to confirm what has been long suspected. It isn’t the end of the research trail, by any means, but it is an important step along the way in our understanding of how novel influenza’s affect the human host. More studies, undoubtedly, will be needed.
Doctors can hopefully use the information garnered from this research to work on ways to combat this cytokine storm. It won’t be easy. Attempts to dampen down the body’s immune system using steroids, or other methods, entail other dangers. Secondary bacterial infections, such as pneumonias, could flourish if the immune system is suppressed, and the virus could replicate unchecked. Additionally, the drugs used to suppress the immune system have serious side effects.
Still, this is important work, and represents real progress in our battle to learn as much as we can about the next pandemic before it comes.
