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Apr 25, 2013
 |  BC Innovations  |  Targets & Mechanisms

Interfering with interferon

Type I interferon receptors are key factors that promote antiviral immunity, but two separate teams have found that elevated interferon signaling may actually be detrimental to the body's ability to fight persistent infections. Groups at The Scripps Research Institute and the University of California, Los Angeles showed that blocking type I interferon during the persistent stages of viral infections in mice can resolve the infections.1,2

One key implication from the findings is that researchers should re-evaluate how to use interferon in treating HCV, as it has important antiviral benefits in acute infections but may be damaging during persistent infection.

According to David Brooks, who led the UCLA team, "There is a growing idea that dampening the constant immune activation in chronic infectious diseases has benefits. Our idea that interferon may be driving persistent infections adds one more piece to the puzzle." Brooks is assistant professor of microbiology, immunology and molecular genetics at UCLA.

Type I interferon is secreted by multiple cell types, including immune cells, and plays a key role in the antiviral immune response. Many acute viral infections are cleared by the antiviral cytotoxic T cell response that involves interferon signaling.

But some viruses, including HIV and HCV, establish persistent infections by wearing down the immune system via chronic inflammation and T cell exhaustion or by evading the immune system through the upregulation of immunosuppressive factors that dampen antiviral immunity.

Indeed, previous studies have shown that upregulation of immunosuppressive factors such as programmed cell death 1 ligand 1

(CD274 molecule; PD-L1; B7-H1) or IL-10 contribute to chronic infections and cancers,3 and other work suggests that chronic inflammation contributes to chronic infection.4

Now, two separate teams have built on the prior findings by examining immune system dysfunction in chronic diseases. Both teams...

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