Hmm my virus traps work seems to be generating quite a bit of interest. I originally thought it was kind of a neat idea, but just a special case of a broader research program I've been involved in: bacteriophage growth in environments containing multiple host types.
However the virus trap idea seems to have captured the popular imagination. First, Carl Zimmer wrote about virus traps for the NY Science Times. Then the we the German public broadcaster ARD contacted my former PI about including a segment about virus traps in a series of documentary films about viruses. (No word yet whether they will go thru with it; as the director mentions, it might be difficult to "find a 'visual' way to explain your work"). Finally, Janet Ginsburg wrote about virus traps for New Scientist. (Unfortunately it is not open access so go buy a copy at your newsstand or get 4 issues for $4.95 if you purchase online). Janet promises to write about it for her excellent blog as well. I, for one, am eagerly waiting the article.
In the meantime, I've copied a quote from the article.
"Tackling the issue from a different perspective is ecologist Paul Turner of Yale University. To him, a virus trap is an example of an 'ecological trap' - a habitat that looks fertile but is actually a blind alley. The classic example is mayflies mistaking asphalt for water and laying their eggs on it. In nature, ecological traps can cause local populations to decline, or even die out if they outnumber fertile habitats. Turner wanted to know under what conditions artificial virus traps could do the same, so he created a mini-ecosystem made up of the bacterium Pseudomonas syringae and a virus called phi 6, which preys on it (Ecology Letters, vol 10, p 230).
He chose this system because it is easy to introduce a trap. To attack Pseudomonas, phi 6 first latches onto telescopic appendages called pili, which the bacterium uses to invade plants. When the pili are retracted, the virus is pulled inside. However, there is a mutant 'superpiliated' strain of Pseudomonas which has more pili than normal but cannot retract them, meaning phi 6 can bind to but cannot enter and infect the bacterium. This is the strain used to trap would-be invaders.
To test its effectiveness, Turner prepared test tubes of the bacterium with varying levels of trap, then introduced the virus. 'We set up a game playing by the simplest rules possible,' he explains. He judged success or failure by viral survival and growth rates. If the trap works, virus levels should decline - which is exactly what happened. A 50:50 mix of traps and normal bacteria vanquished phi 6 completely.
Turner's team is now looking to turn experiment into therapy, removing red blood cells and adding decoy attachment sites for viruses. Their focus right now is HIV. 'All of our drugs against HIV are effective because they keep immune cell counts up,' says Turner. 'That's a very expensive venture that a lot of people can't afford. If you could find a way to protect those cells through a sheer onslaught of traps, that might be another way to achieve the same thing.'"
Photo of HIV budding from a CD4 cell from NIH.