It's a fascinating field because you have to look at both the evolution of the virus, but also the evolution of the immune response against the virus. In many cases it is that back-and-forth evolution.
We know quite a bit from the original SARS as well about which receptors on the surface of a host cell or human cells allow the virus to bind and get in, but we're also learning that there's more than just one. Now that we recognize some cell types don't express the protein that is normally the receptor, it's becoming more interesting to understand what the other receptors are, what particular cell types that protein is on, and that starts to explain some of the other symptoms we're seeing.
We have indications of gastrointestinal potential—and it's still being tested—but we certainly at McMaster, and I know of others, are looking at the possibility of transmission in live virus, for example, in feces from the gastrointestinal tract.
As we understand more about what cells the virus can get into.... In some cells, the virus can't make copies of itself, but the cell will still respond. The cell can still make certain cytokines that will show symptoms, or that can induce certain symptoms even if that cell doesn't allow for viruses to make multiple copies of itself.
The more we get to understand the biology, the more we're starting to very slowly understand some clinical symptoms.