Technology Background

The body’s response to a viral infection can be divided into an immediate innate immune response and an adaptive immune response. The innate immune system is a rapid, non-specific defense against infection and is characterized by inflammation. The adaptive immune system is a specific response to infection and is triggered by the innate immune response. To novel viruses, the adaptive immune response can take days to mount an effective response and eliminate a virus.

The presence of a viral infection in the lungs is detected by the binding of a pathogen-associated trigger (PAT), as dsRNA, to a toll-like receptor (TLR). During the early acute response to virus infection, PAT binding sends specific molecular signals to ramp up the expression and release of pro-inflammatory mediators, including cytokines and chemokines. Upon release, cytokines activate additional immune cells to mount an attack on the infection. Chemokines attract additional immune cells to the site of infection. In this way, an intense, local response is launched at the site of infection.

During a well-tempered response to infection, the inflammatory response is dampened by the removal of PATs and decreased production of cytokine and chemokine production, as well as, the production of anti-inflammatory molecular signals.

Unfortunately not all responses to influenza infection are well-tempered. Recent media reports of infections by new Influenza A H5N1 (bird flu) and A H1N1 (swine flu) tell of many patient deaths. The deaths apparently can be due to a “cytokine storm” caused by pathological inflammation with the excessive production of cytokines and chemokines which can lead to the accumulation of white blood cells in the lungs and decreased lung function. In addition, release of cytokines outside of the lungs can lead to systemic inflammation, organ failure and ultimately, death.