Sam Sanderson from the University of Nebraska and his colleagues from various San Diego institutions may have found a new weapon in the war against the flu. To explain, let's take a look at our immune system.
Perhaps the most well known component of our immune system involves the ‘acquired immune response’ in which each tiny invader is attacked by specific antibodies. However, there is also an ‘innate immune system’. Briefly, upon encountering pathogens, the body quickly releases protein cues that encourage immune cells to flock to the area and contain the infection until more troops can be summoned to dispose of the bugs. Unlike the acquired immune response, the innate system is nonspecific. As such, it can be initiated much more quickly. Where it may take a few days for antibody assembly to go into full production, the innate response takes only hours.
One of the components of innate response is the glycoprotein C5a. The binding of C5a to its receptor is a key occurrence in the cascade of events that results in the innate response. Blocking this receptor has a deleterious effect on mice suffering from influenza.
There is a synthetic version of human C5a called EP67. Sanderson and his colleagues found that chemicals involved in the innate immune system were released within two hours of administering EP67 to mice. More importantly, 100% of mice given EP67 within a day of infection with a lethal dose of influenza survived that infection.
This is particularly significant because influenza is a tricky little bugger. The virus can actually suppress the immune system for up to 48 hours, meaning that most hosts will suffer from the full-blown and highly shareable symptoms we associate with having the flu. EP67 seems able to circumvent this delaying tactic.