How Immune System ‘Scars’ Make Flu More Deadly
U. Melbourne, 15 Nov 17

(Credit: Getty Images)

New research sheds light on why patients who survive a severe infection or physical inflammation, such as pneumonia from the flu, may be more vulnerable to secondary infections in recovery.

“This new knowledge is changing our thinking about how best to manage patients after their infections.”

Researchers discovered that the initial infection paralyzes our immune system, inhibiting its ability to fight off subsequent infections. The findings raise questions about treatments inside Intensive Care Units (ICU) following acute infection, sepsis (inflammation), and even severe trauma.

“Flu deaths are commonly caused by lower respiratory tract infections and pneumonia—a leading cause of death from infectious disease,” explains research leader Jose Villadangos, who is based jointly at the Peter Doherty Institute for Infection and Immunity and the Bio21 Institute at the University of Melbourne.

“The risk of pneumonia is particularly high for critically ill patients recovering from their first flu infection episode,” he says. “After an initial severe infection, patients may be at high risk of contracting secondary infections and developing fatal pneumonia.”

“We have discovered that recovery from the viral infection leaves an ‘immunological scar’ that reduces the immune system’s capacity to launch protective responses against subsequent infections,” says Villadangos.

Immune system malfunction

“We are not evolved to survive the level of inflammatory assault that would send a person to ICU. Modern medicine in ICU is the only reason we survive,” Villadangos explains. “But this comes at a cost: the same processes that are normally at work to stop inflammation after the resolution of infection, ‘overshoot’ in ICU survivors, leaving them immunosuppressed.”

It means that as a person recovers from their primary infection, their immune cells are less able to activate their immune system.

“We have termed this phenomenon ‘immunological paralysis,” Villadangos explains. “This new knowledge is changing our thinking about how best to manage patients after their infections.”

The research, based on tests in mice and observations in patients, was led by Villadangos with Antoine Roquilly, who is now based at the University Nantes in France.

“We found that, following a primary infection, immune cells became ‘paralyzed…'”

To uncover the mechanism for the immunosuppression, the researchers measured the levels and activity of immune cells responsible for fighting infection.

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