I don't think you and I are saying the same thing. There are emerging views that with a larger portion of the population being asymptametic (potentially as high as 50%) and just general underst-estimating of the overall count (much more so than initial estimates), that the mortality rates may be massively elevated (still well in excess of the flu so I'm not doing some flu comparison here). Obviously...if you don't social distance, you have more infected, hospitals crash, and mortality skyrockets (but that is a different variable driving the mortality than the variable I am discussing). That said...basic math says if I think 1 person dies out of every 100 (if hospitals are safe) but instead, it is actually 1 person per 1000...you end up at a dramatically different point of the basic mortality curve. And from there, you tweak mortality based upon the stress & capacity of the hospitals, including relevant equipment, etc to treat and ventilate, etc.
You have to look at all the independent factors and then when you run the model, you blend in the components to come up with new projections. Social distancing is the single biggest reason we have contained it and you can't lax very much. The widely held wisdom is you need 90% social distancing to shut this thing down in 3 months (doesn't mean you have killed it...but that is what you are probably talking about). If you are only at 80% of population doing Social Distancing...it is going to take 4 months. Anything 70% below and you just flat out won't contain it. That is why it will be paramount once we do knock this down that everyone is ready to rapidly identify and respond (including rapid shutdowns of borders, etc) until they actually have a cure and/or an effective way to treat this thing. Further, the R0 has been fundamentally lowered due to this measures (moving from 2.5+ to 0.6). R0 < 1 would indicate the virus will continue to dwindle and eventually die-out over time.
To go a little deeper, there is also emerging research being done on select comorbidities and what is driving such the high rates of mortality within subsets of the population and an emerging UK study is believing the COVID virus is getting into the body by latching on to ACE2 receptors. Specifically patients with hypertension, diabetes, and other cardiovascular diseases tend to take groups of drugs which are known as Ace Inhibitors and/or angiotensin receptors, which cause an individual to put out more ACE2 receptors, which increase their susceptibility to the infection (and depth of the infection). This only explains these particular comorbidities, but obviously research is being done broadly and who knows whether any of this holds or not.