A just-so story

 SARS-CoV-2 is not a bat disease; it reproduces in humans, and is a human disease.  It's descended from a bat disease, and may thereby retain some characteristics of bat diseases.

Most bats are tiny and have trouble meeting their metabolic needs; you'll see stylised facts about how bats can eat their own body weight in insects every night, and so on.  What this means to a bat is that it is bradymetabolic, with two metabolic states; the fast one for flapping around, actively hunting flying insects, and the slow one for roosting.  If the bat (tiny, big heat loss area from its skin-covered wings) tried to maintain the fast metabolism all the time, it would starve to death because it couldn't eat enough to get itself through a long summer day.

What this means for bat viruses is that they're a virus; they don't have enough DNA or RNA to carry one set of biochemical machinery for the warm temperature and one set for the cool temperature.  It's one or the other.  Either way, the bat won't stay in that state for long; it will switch by going out to hunt or to come in to roost, and then the virus gets subjected to the equivalent of a high fever or a medically induced coma depending on whether it's got the biochemistry for conditions in a cool bat or a warm bat.  It means bat viruses are hasty; the time window to reproduce enough to spread is short.

COVID-19 isn't that contagious, except when it is; a disease that doesn't spread very well most of the time spreads like measles sometimes.  The average comes out to worrisome, but the distribution has a "meh" arm and a "red alert!" arm.

We're not bats.  We are automatic endotherms; we're not as warm or as cool as a bat. The "go for it, go for it, now now now" mechanism in SARS-CoV-2 doesn't trigger all that often or all that reliably.  When it does, and the person the virus is going into maximal-shed-mode in happens to be inside with other people, we get a super-spreader event.

One also has to note that the super-spreader events we know about don't correlate to anything in terms of the person who arrives infected; the event requires people being inside, lots of talking, poor air circulation, etc., but there's absolutely nothing about the infected person that indicates why they might be a greater source of contagion.  In this just-so story, it's pure bad luck; their infection happened to trigger "go for it!"  mode at just that time.

Couple-three things to watch out for:

1. Some estimates put 80% of the total number of COVID-19 infections as happening due to super-spreader events.  That's an obvious source of selection pressure to produce strains of SARS-CoV-2 that are better at triggering their "go for it!" levels of shedding in humans.
2. severity of the disease correlates with viral load; a virus strain better at doing rapid reproduction in humans will move the average dose up in those infected by shedding more on average compared to current strains
3. further adaptation to humans includes the possibility of an always-on strain of SARS-CoV-2

I'm not kind of medical professional, biochemist, or virologist.  I don't know any of this applies; it's a just-so story built out of public statements about how bat viruses in general and SARS-CoV-2 in particular work.  And for all my numerous character flaws, optimism is not one of them.

Still find myself much inclined to avoid taking chances this boreal winter.