When looking to biology for inspiration on computer security, it is natural to first look at mammalian immune systems. While they are amazingly effective, they are also mind-numbingly complex. As a result, many researchers get seduced by the immune system’s architecture when there is so much to learn from its lower-level workings.
Case in point: every cell in the human body can detect many kinds of viral infection on their own, i.e., with no assistance from the cells of the immune system. As this recent article from Science shows, we are still far from understanding how such mechanisms actually work. My high-level take on this article, as a computer security researcher, is that:
- Basically all cells in mammals (and, I think, most animals in general) can generate immune system signals that generate responses from internal and external mechanisms. A key source for such signals is foreign RNA (code) inside the cytoplasm of a cell. Of course, there is a lot of other, “self”-RNA in that cytoplasm as well – so how does the cell tell the difference between them?
- A key heuristic is that native RNA is only copied in the nucleus of a cell; RNA-based viruses, however, need to make RNA copies in the cytoplasm (that’s where they end up after getting injected and it isn’t easy to get into the nucleus – code basically only goes out, it hardly ever goes in). RNA polymerases (RNA copiers) all use the same basic patterns to mark where copying should start. Receptors such as RIG-I detect RNA with “copy me” signals (5′-PPP) in places where no copying should occur (the cytoplasm).
- Of course, this is biology, so the picture isn’t so clear-cut. A simple “copy me” signal won’t trigger a response; there must also be some base pairing – the RNA molecule must fold back on itself or be bound to another (partially complementary) RNA molecule. I’d guess this additional constraint is there because normal messenger RNA is strictly single-stranded. (Indeed, kinks or pairing in messenger RNA are bad in general because they’ll interfere with the creation of proteins.)
Of course, all of this is partial information – there’s evidence that these foreign RNA-detecting molecules (the RLR-family) trigger under other additional constraints. This doesn’t surprise me either, as this mechanism must operate with extremely low false positives; one or two matching rules aren’t up to the task given the complexity of cellular machinery and (more importantly) given the evolution of viruses to circumvent these protections. Viruses have evolved ways to shutdown or suppress RLR-related receptors. Although cells will be pushed to evolve anti-circumvention mechanisms, in practice this is limited in the cellular environment—make the detectors too sensitive and a cell will kill itself spontaneously! The solution has been to keep a circumventable but highly accurate detector in place; the arms race instead has moved to optimizing the larger immune system.
I leave any conclusions regarding the design of computer defenses as an exercise for the reader. 🙂