That may be because she swabbed her tonsils as well as her nostrils for the first time today.
A lag of two or three days from symptoms to rapid tests showing positive has been characteristic of omicron for some time. There's maybe some evidence to suggest BQ.1 and BQ.1.5 may be a bit more challenging for rapid tests than previous variants but the way that usually goes is the data's not in and analyzed until after a wave has passed.
I've come across many calls to update rapid tests to omicron, which seems reasonable enough to me. However, I've stopped following the back and forth on that since there hasn't appeared to be much interest from the parties capable of actually making an update happen. But hopefully something's getting done and I'm just not aware of it.
There's no law which says this must be the case, but my understanding is that viruses such as influenza and coronavirus generally mutate and adapt through time to become more easily spread and less lethal to the host.
I'm afraid the last bit's it's more of a common misunderstanding. The selection pressure for viruses is very much to spread and, if their host dies after infecting a bunch of others, that's a longer term thing which doesn't usually have much of an effect. We've seen that plenty with SARS-CoV-2, for example, where hospitalizations and deaths consistently lag infection waves and BA.1 doubled to quadrupled death rates.
Reconstruction of 1918 H1N1's genome offers another perspective, by comparison with currently circulating genomes and sequences from post-1918 flu epidemics. Doesn't seem to be much an inverse relationship between spread and lethality. If anything maybe the opposite. But it's a little hard to tell since higher spread and higher lethality both create greater variant awareness, increasing the chance of being able to get historical samples to sequence. There's also been a lot of ancient DNA recovery of
Yersinia pestis and, whilst it's a bacterium, those efforts make it another reasonably good source on this. Similar results, from what I understand, though it's been a couple years since I last looked into plague studies.
On the host side, yes, there's selection pressure to adapt to make the virus less debilitating. The primary adaptation mechanism, however, is removal of less resistant hosts from the gene pool through mortality. So it's not a fun process for the hosts and, to the extent one's susceptibility to SARS-CoV-2 is determined by genetics and aging, there's nothing you can do about it. What one can do is layer protection—vigilance, ventilation, distancing, masking, vaccination, and staying in the best health you can manage—which isn't evolution in the classic sense. But it is a suite of adaptations which better one's odds.
Descendants of the 1918 influenza virus (which killed more people than the First World War) still circulate today, so I think it's a safe bet that Covid 19 will be with us long term.
Yup, see
Souilmi et al. 2021 for example. Only exception so far is smallpox, and even that's potentially temporary should someone decide to pull it out of a weapons vault.