"So COVID-19 is ( paraphrasing the simpler version from Don)  "attaching to human cells by utilizing BRD-4 ... After it’s attached, it uses human receptors, one of them called ACE2 and another TMPRSS2, and.... Apabetalone causes a huge reduction of ACE2 and some other receptors,  as they are inflammatory markers..."

That statement is misleading, in my opinion. There is no proven role for the virus directly attaching/using BRD4 for infection/entry into the cell. Instead, it is indirect through transcriptional control of genes such as ACE2 and TMPRSS2. ACE2 is a receptor for the virus spike protein and TMPRSS2 is a protease that acts to cleave the spike protein in a "priming" step that facilitates fusion of the viral and cellular membranes.

"So my question is... how common is this pathway among viruses? Is it common among the whole family of corona viruses? Is it rare and unique to COVID-19? Because IF this is a common pathway for a whole herd of infectious viral (or maybe even other) agents, the implications of these findings could be more significant than if it is only applicable to COVID."

A quick google search reveals that the role of ACE2 and TMPRSS2 seems to be common to coronavirus family members beyond just SARS-CoV2 and including at least SARS-CoV and MERS-CoV. This is not my area of expertise, so I do not know if there is a known role for ACE2 and TMPRSS2 beyond the coronavirus family.

https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.120.15256

https://www.sciencedirect.com/science/article/pii/S0092867420302294