The first is that we have a strong mechanism story we can tell. Viruses take time to multiply. When the immune system detects a virus it responds. If your initial viral load is low your immune system gets a head start, so you do better.
The problem with this story is that it assumes that immune system detection time is not dependent on viral load, which seems highly unlikely. The more viral particles, the more likely they will be detected. How that interacts with viral load’s more obvious direct effects is complex and probably virus strain dependent.
The second category is the terrible outcomes in health care workers on the front lines. Those who are dealing with the crisis first hand are dealing with lots of intense exposures to the virus. When they do catch it, they are experiencing high death rates.
Evidence/source?
Your third category on analogy evidence from other viruses makes sense, with the single example from the other SARS coronavirus carrying more weight as it’s a much closer relation than smallpox or measles.
The problem with this story is that it assumes that immune system detection time is not dependent on viral load, which seems highly unlikely. The more viral particles, the more likely they will be detected. How that interacts with viral load’s more obvious direct effects is complex and probably virus strain dependent.
Evidence/source?
Your third category on analogy evidence from other viruses makes sense, with the single example from the other SARS coronavirus carrying more weight as it’s a much closer relation than smallpox or measles.