Very realistic possibility. However from a strictly scientific mindset we have to rule out ALL other possibilities for the higher death rate in the apartments, which the article does not.

Many other variables to account for.

Air quality in the building that may have compromised the tenants. Just like smokers are more susceptible to Coronavirus. Air quality issues could have been at play. Cironavirus affect airway tissue, or tissues with ACE2 receptors.

So it’s a little over simplistic to conclusively state the viral load was higher from a single dude breathing on the same building. Don’t think that could be proven effectively.

The thought has merit. It is reasonable to think a lower infectious dose can give a small amount of time for the immune system to prime.

I reason that after a few replication cycles the viral load is so great as to overwhelm the system or available receptors to make it a moot point. (Perhaps I am wrong)

I inquired with my MD molecularbiologist colleague, thinking I was loosing my mind.

He agreed that a higher initial dose might hit harder at first, but the exponential replication of the virus makes those numbers immaterial in the bigger picture.

I believe the most significant variance to the levels of infection do not come from viral infectious dose, initial viral loads, or variances in viral genome. I believe it has more to do with the hosts affinity for the virus (more ACE2 receptors), health status, and immune system ability to fight properly.