Los Angeles:  Temporarily blocking a protein critical to immune response may help the body clear itself of chronic infection such as HIV and hepatitis C, a new study has claimed.
The finding, published in journal Science, suggests new approaches to treating persistent viral infections like HIV and hepatitis C, University of California Los Angeles (UCLA) scientists have shown.
The research team studied type-1 interferons (IFN-1), proteins released by cells in response to disease-causing organisms. These proteins enable cells to talk to each other and orchestrate an immune response against infection.     Constant IFN-1 signalling is also a trademark of chronic viral infection and disease progression, particularly in HIV.
"When cells confront viruses, they produce type-1 interferons, which trigger the immune system's protective defences and set off an alarm to notify surrounding cells," said principal investigator David Brooks.
"Type-1 interferon is like the guy in the watchtower yelling 'red alert' when the marauders try to raid the castle," Brooks said in a statement.
Scientists have long viewed IFN-1 as beneficial, because it stimulates antiviral immunity and helps control acute infection. Blocking IFN-1 activity, they reasoned, would allow infection to run rampant through the immune system.     

On the other hand, prolonged IFN-1 signalling is linked to many chronic immune problems. The research team wondered whether obstructing the signalling pathway would enable the immune system to recover enough to fight off chronic infection.
To test this theory, Brooks and his colleagues injected mice suffering from chronic viral infection with an antibody that temporarily blocked IFN-1 activity.
Much to their surprise, they discovered that giving the immune system a holiday from IFN-1 boosted the body's ability to fight the virus. Stunningly, the respite also reversed many of the immune problems that result from chronic infection, such as a rise in proteins that suppress immune response, continuous activation of the immune system and disruption of lymph tissue.     The findings fly in the face of past studies that suggest eliminating IFN-1 activity in mice leads to severe, lifelong infection.
"What we saw was entirely illogical. We'd blocked something critical for infection control and expected the immune system to lose the fight against infection.
"Instead, the temporary break in IFN-1 signalling improved the immune system's ability to control infection. Our next step will be to figure out why and how to harness it for therapies to treat humans," Brooks said.