ALBANY, N.Y. (The New York Times News Service) -- A discovery by Albany Medical College researchers here may finally explain why people sometimes get a strain of influenza that seems to last forever.

The medical community has long known that a bout of the flu makes people more susceptible to a secondary bacterial infection like bronchitis, ear infection, pink eye and pneumonia. The second infection often emerges about a week later, when the patient starts to feel better.

A team led by professor Dennis Metzger found that, in mice, a molecule called interferon is released as part of the immune response to fight the virus; but it inadvertently turns off the body's defenses against the pneumococcus bacteria.

"Things return to normal after a week or so, but not before bacterial infections have been given a window of opportunity," said Metzger, director of the Center for Immunology and Microbial Disease at Albany Med. The team's research and proposal for a cure were published online Sunday in the journal Nature Medicine.

Bacterial infections can be more severe than the viruses. During flu pandemics, like the infamous 1918 outbreak, at least half the people who died succumbed to secondary infections, not the flu itself, Metzger said.

Scientists have been trying to find the link between viral infections and secondary bacterial infections for years. Metzger's team is the first to demonstrate a mechanism.

"It gives us totally new insights into how this interaction between influenza and the pneumococcus is taking place," said Dr.

Keith Klugman, a professor of global health at Emory University in Atlanta and leading expert on the pneumococcus infection.

The lung has cells called alveolar macrophages, which protect the body from bacteria that are inhaled. About six or seven days into a viral infection -- like flu or a common cold -- the macrophages are turned off by the release of interferon, at about the time that bacterial infections take hold.

Metzger's team found that treating mice with interferon antibodies rendered interferons useless, and the mice did not develop secondary infections.

"Yet even without the help of interferon, the immune system was still able to properly fight off the (flu) virus, leading us to think that maybe interferon is not playing a central role in the anti-viralimmunity," he said.

It isn't clear if the research will apply to humans, but Metzger said the influenza infection in mice closely mimics the human version.

An antibody treatment would provide an attractive alternative to traditional antibiotic therapy. Antibiotics are drugs that kill bacteria, but the bacteria are becoming resistant to them.

Antibodies are proteins produced naturally by the body's white blood cells and they can inactivate or destroy bacteria.

Albany Medical College holds a provisional patent to the new treatment therapy and Metzger said he hopes to partner with a pharmaceutical company to conduct clinical trials.

"This is very promising," said Klugman.

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