Washington, May 21 (IANS) Researchers have identified a critical molecular mechanism that allows the flu virus to evade the body’s immune response system.
“We have found a mechanism that the influenza virus uses to inhibit the body’s immune response,” said Jae Jung, professor in molecular microbiology at University of Southern California (USC), and the principal study investigator.

“This finding could provide researchers with the information needed to create a new drug to enhance immunity and block influenza virus infection and replication,” Jung added.

Several specific intra-cellular receptors are responsible for detecting the virus and activating the body’s defensive mechanisms.

When a virus’ RNA enters the intra-cellular fluid, a receptor known as retinoic-acid-inducible gene I (RIG-I) detects it and triggers a response that limits virus replication and calls the body’s defences into action.

RIG-I acts as the sensor and security force against attacks, Jung explained. Then, a protein known as TRIM25 helps RIG-I transmit an alarm signal, which ultimately floods the cell and surrounding tissue with antiviral interferons.

The flu virus is highly infectious and poses a serious and sometimes deadly health risk because of its ability to mutate into new strains and spread quickly during seasonal epidemics, as seen in the recent outbreak of the H1N1 swine flu virus, Jung said.

Researchers have long been working to understand how respiratory influenza is able to slip past the body’s immune responses. They have found that the influenza A virus has evolved by incorporating Non-structural protein 1 (NS1) into its genome to escape the RIG-I alarm system, said an USC release.

This process is one reason why the virus kills an average of 36,000 people every year. In fact, the 1918 ‘Spanish flu’ pandemic flu virus, which killed over 40 million people worldwide, muted the RIG-I response and interferon (cell signalling proteins) activity much more efficiently than contemporary flu viruses, Jung notes.

The study was published in the May 21 issue of the journal Cell Host & Microbe.