Three points.

It would appear that at any stage of infection, the effect of ABL on clinical outcome will be determined by the relative impacts of the drug on receptor expression and viral replication. When viruses multiply inside infected cells, the cells eventually burst to release them, and they go on to infect more cells. But that reinfection of new cells is via the same type of receptor, which if sufficiently suppressed won't let the viruses in.

Second, it seems the paper has not yet been peer reviewed by other academics.

Third, if it turns out that ABL is good at preventing infection, but does not exacerbate an existing infection, it might give it a very big market as a prophylactic, perhaps even greater than as a therapeutic. This of course would need to be tested in another trial.