While we should at least ask and assess that question...
Yes, it would be good to rule out those things that we do know to expect. And I think animal results* could check this one somewhat. But corners are already being cut, and I still expect some degree of surprises.
I do feel like there’s a lot we don’t know with this virus. I don’t know that the problems will be limited to the things we currently know to look for, and I’d be a little surprised if timing was not at least a bit of an influencing factor.
* Apparently they haven’t found/developed an easy animal that catches the virus, but they are doing animal testing in parallel to check the type of immune response? And the vaccine test result with the 4 macaques at least seemed promising, now up by another 10 macaques tested with that same inactivated-virus vaccine.
While it definitely helps that we have some experience with SARS-1, we can’t totally rely on what we know about SARS-1 and trust that it’ll apply to SARS-2.
(I think SARS-1 and SARS-2′s genetic similarity was said to be only ~80%? This is about as much as we share in common with cows. There can be meaningful differences between the two.)
Here’s just one example. Did you see the “UPDATE” I added to my answer above? Says something like “Oh hey, I guess it probably does make immune cells apoptose?” SARS-1 doesn’t do that thing. As in, the article specifically mentions that they tried with SARS-1 and SARS-2, and only SARS-2 gets into T-cells like this. And they weren’t sure which receptor was responsible.
It’s great to see a lot of science happening on this, but it’s also something of a marker of our vast uncertainties paired with its high priority.
While we should at least ask and assess that question...
Yes, it would be good to rule out those things that we do know to expect. And I think animal results* could check this one somewhat. But corners are already being cut, and I still expect some degree of surprises.
I do feel like there’s a lot we don’t know with this virus. I don’t know that the problems will be limited to the things we currently know to look for, and I’d be a little surprised if timing was not at least a bit of an influencing factor.
* Apparently they haven’t found/developed an easy animal that catches the virus, but they are doing animal testing in parallel to check the type of immune response? And the vaccine test result with the 4 macaques at least seemed promising, now up by another 10 macaques tested with that same inactivated-virus vaccine.
While it definitely helps that we have some experience with SARS-1, we can’t totally rely on what we know about SARS-1 and trust that it’ll apply to SARS-2.
(I think SARS-1 and SARS-2′s genetic similarity was said to be only ~80%? This is about as much as we share in common with cows. There can be meaningful differences between the two.)
Here’s just one example. Did you see the “UPDATE” I added to my answer above? Says something like “Oh hey, I guess it probably does make immune cells apoptose?” SARS-1 doesn’t do that thing. As in, the article specifically mentions that they tried with SARS-1 and SARS-2, and only SARS-2 gets into T-cells like this. And they weren’t sure which receptor was responsible.
It’s great to see a lot of science happening on this, but it’s also something of a marker of our vast uncertainties paired with its high priority.