Thanks Bear and Golf,

This is a bit of a long shot:

According to this paper:

https://www.sciencedirect.com/science/article/pii/S2211124713005639

the murine leukemia virus integrates into the host genome (for replication) near histones with attached BRDs.  So BETis (which knock the BRDs off histones) prevent viral integration and therefore replication.  From the paper:

"Although HIV integration site targeting is mediated by LEDGF/p75 (Cherepanov et al., 2003, Ciuffi et al., 2005, Gijsbers et al., 2010, Llano et al., 2006, Schrijvers et al., 2012, Shun et al., 2007), the cellular cofactor driving MLV integration site targeting remained unknown. Here, we describe BET proteins as the MLV targeting factors. In agreement with Sharma et al. (2013), we show that BRD2, BRD3, and BRD4 specifically interact with MLV IN and that bromodomain inhibitors can block MLV replication at the integration step."

So, perhaps SARS-CoV-2 also requires a BRD location in the chromatin to for integration and/or replication.  By knocking BRD2/BRD4 molecules off hstones, apabetalone would reduce the number of integration sites.  Not clear whether either of BD1 or BD2 is involved in the MLV viral recognition of BRDs, it might be some moiety outside the BDs.

Jupe