A weaponized strain would be designed deliberately to be indistinguishable from a natural origin, so there will be no proving that without documents or a confession. An incidental genesis would be an intentional chimera, produced just for research, that got loose. An accidental genesis would be very like a natural origin, but just in lab animals based on strains handled in the lab, maybe even mixed with a natural strain brought in by accident, even incubated unbeknownst in a lab employee.
Personally, I doubt we will ever know more than we do now. All four are possible, all four should be guarded against in the future. But guarding against weaponized viruses is arbitrarily hard. Russia probably still has casks of weaponized smallpox stored underground somewhere. US and China, too, possibly.
To me, the "strength" of the covid-19 is evidence of successful lab experiments, not a fluke contagion. As the pandemic variants showed, natural evolution of viruses tend toward being less lethal. So why did Sars-Cov-2 start overpowered and get weaker?
As viruses can make the jump from one species to another, then it should not be hard to imagine how easy it would be to engineer that same outcome; that is all "gain of function" experiments do: try to emulate a pipeline for viral mutation.
That virulence (contagiousness) is also evidence though. Yes, an airborne respiratory viruses needs to be more contagious than other types, and a more contagious virus needs to be less deadly, or natural selection is going to do its thing (people die before spreading it). Sars-COV-2 was LESS contagious and more deadly than a typical respiratory virus. That is called evidence.
Smallpox was overwhelmingly more deadly, and its spread was not limited, even without airborne transmission. Measles was also overwhelmingly more deadly, did rely on airborne transmission, and afflicted us century in and century out.
Research into viral function, absent military intent, has no reason to experiment with making the infection more deadly. The primary research goal is to discover what may affect virulence, and try to anticipate and understand what may occur naturally, and then discover ways to block those.