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.
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.