Yes, that is my point.
A couple of years ago clinicians decided to change the 'Sepsis' label to 'SIRS' -- systemic inflammatory response syndrome. No real objection from me, but the immune response tracks quite well with circulating bacterial cell wall LPS. Meaning SIRS tracks with septicemia. My ER friends would routinely tell me about patients that came in ill but stable and shortly after receiving antibiotics would crash. This was a flood of LPS. If you want to watch it in real time, just give Abx to a patient with a high load of spirochetes. You might know the clinical label for the phenomenon.
HOWEVER, with very, very few counter examples, clinical interventions designed to suppress the immune response lead to inferior outcomes. One of the more recent and widely published examples was using the blood product activated protein C (APC). No clinician in their right mind would administer TNF or IL-2 blockage to SIRS patients. The only prominent exception I can think of at the moment is the administration of steroids in severe pneumonia. It is in vogue these days but I am old enough to be wary of fashion medicine. The pendulum has been swinging back and forth on that one for decades but the clinical differences either way are small.
In general (but not always) the body does a find job modulating the immune response to be proportional to the infection, and the immune response is always a double-edged sword. However, it is quite rare for clinicians to do better when they decide to either rev up or down (or both at the same time) the natural response.
Back to basics: Covid-19 severe morbidity and mortality is mostly a disease heralded by existing co-morbidities. It should not surprise you that SIRS is poorly tolerated with clogged coronary arteries. Do you have any ICU experience ? Mine spans a couple of decades after I left academic medicine and I can tell you that co-morbidities sets the stage for the lion's share of severe infectious disease. Not all.