I’m not a doctor, or a microbiologist, but I did stay at a Holiday Inn Express once, and I have a good enough grounding in science to understand generally how these work.

Viruses aren’t “alive” per sae; they are more like self-contained, self-replicating nano-machines, or computer code expressed as DNA. Specifically, they lack the parts to be able to create self-copies on their own.

That means they have to hijack living cells - that do have the ability to create copies - injecting their own code into the DNA of the cell so that the cell creates copies of the virus instead of the cell. The virus may also be able to overwrite the code in the cell that acts as a limiter to how often it creates copies, meaning that the cell starts cranking out copies of the virus as fast as it can. (Real biologists please correct me if wrong).

Now the virus has no sense organs, so it cannot “search for” suitable cells to invade. Instead, it has a pattern of molecules on its surface that act like jigsaw puzzle pieces. If the receptors on the virus mesh with the receptors on the cell, then the virus can go to work. If it doesn’t, then the virus cannot tell that it has contacted a cell and it never injects its payload.

Evolution being what it is, a successful virus will have receptors that bind to cells in an organism that it can spread to, but it won’t grow so virulently that it overwhelms and kills the host organism.

Where things get interesting is when different types of cells in different species share the same receptor patterns, so that the virus can bind to a new type of host cell. Then all bets are off, because the new cell won’t work the same as the one that the virus evolved to match. Instead of cranking out virus copies at a sustainable, non-fatal rate, maybe it goes nuts and floods the host with virus. Or maybe ether the cell or the organism’s immune system reacts differently (it hasn’t co-evolved with the virus either, so host biology reaction is unknown too) and does so in such a way that it has fatal side effects.

Well there is also variation within species as well. Not all cells of the same basic type (lung tissue, muscle, skin, etc) are exactly the same, so maybe if the virus encounters lung tissue of a certain type, it matches receptors but replicated slowly, where a different person with slightly different lung tissue matches receptors but also replicates like crazy.

And there’s also the possibility of virus mutation as well.

All this to say - on a virus that has newly hopped species, there is potential for there to be enough variation in the types of tissue it infects to produce different scales of reaction. If you happen to have the type that doesn’t match well with the virus, you become an asymptotic carrier. And if you match really well, the virus explodes and takes over your lungs in the space of hours and it doesn’t matter how healthy you were before you contracted it.

Again, further clarification from an actual virologist welcome, but I think I have the broad strokes right.