THE “Spanish” flu that killed up to 50 million people in 1918-19 owed its peculiarly devastating symptoms to a huge overreaction by the body’s own defences, research suggests.

The first attempt to infect animals with a reconstructed version of the 1918 virus has shown that it provokes an immune system response that probably explains its deadly effects.

The findings offer important insights into how particularly virulent influenza viruses damage the body, with implications for the H5N1 avian flu and other strains with the potential to cause a pandemic.

Analysis of the re-created 1918 virus has already established that it has similarities to H5N1, although it belongs to a different strain, H1N1.

A team led by John Kash, of the University of Washington in Seattle, used the reconstructed virus to infect mice, and also infected a control group of mice with a less virulent human strain of flu.

The Spanish flu triggered a much more extreme immune reaction in the animals’ lungs, activating genes that kill off infected cells in order to clear the body of disease. Details of the research are published today in the journal Nature.

While this response is normally a critical part of the body’s defences against infection, when it is too strong it can cause as much damage as the disease itself. This could explain why the 1918 virus was so lethal.

“What we think is happening is that the host’s inflammatory response is being highly activated by the virus, and that response is making the virus much more damaging to the host,” Dr Kash said.

“The host’s immune system may be overreacting and killing off too many cells, and that may be a key contributor to what makes this virus more pathogenic.”

By understanding how this immune overreaction takes place, the researchers hope that they may be able to find a way of damping it down, so that infections with virulent forms of flu do not harm the patient. A parallel treatment strategy could then be adopted: an antiviral drug, such as Tamiflu, would be given to kill the virus, while an anti-inflammatory was used to temper the immune system’s activity.

“We’re trying to find targets in the host, instead of just in the virus itself,” said Michael Katze, Professor of Microbiology at the University of Washington, another leader of the research team. “Then you could have a one-two punch that affects the viral infection, but also dampens the host immune-system response.”

Christopher Basler, of Mount Sinai School of Medicine in New York, said: “Our next step is to . . . deconstruct what the immune system is doing so that we can understand why it is reacting so strongly, yet failing to fight the infection. By understanding the trajectory of this particular infection, we may also gain insight into how to treat other types of viral infections that are a threat to public health.”

Global killer

Other flu pandemics struck in 1957 (Asian flu), killing about four million, and in 1968 (Hong Kong flu), killing about one million

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