I'm a typical virologist, I am always talking about interferons. A while ago, under a slightly different guise, I wrote about the biological function of interferon proteins in stimulating the expression of myriad genes, many of which have proven antiviral activity. The fact that these genes and their protein products have antiviral functions makes them extremely interesting to researchers, like me, looking for new ways to treat human and animal infections with these viruses. Or even to anyone really who is interested in viral disease, evolution and medicine. These interferon stimulated proteins are especially interesting for studying viruses for which no vaccine exists. I'm thinking HIV, hepatitis C virus and even emerging infections like Ebola and rabies viruses. And until we develop good vaccines against these agents we're probably going to need antivirals. Note that even if we did have vaccines for these viruses they might not be economically viable to use and so we're back to making antivirals. Either that or we just screw those affected by the viruses. That's not going to happen.
Here's the issue though. Problem is, it takes years and years (major understatement) of research for humans to generate new antiviral drugs. So what if evolution has done the hard work for us? This is where the interferon proteins and their antiviral effectors come in. Turns out, evolution has done the hardwork for us. And this is where this paper, first author John Schoggins, with a host of other authors (many of which also carried out the experimental work) who worked in many labs, mainly across the US. Have a look at the paper for a list. These guys, along with an early paper featuring Sam Wilson and others (see my blog post linked to above), are pioneering the exploration of the - brace yourselves - the 'interferome' with a hope of generating novel antiviral drugs. My words not theirs.
