The problem is not on the HIV replication side, but on the...

The problem is not on the HIV replication side, but on the activation side. It is already possible with the current HIV drugs to completely stop all replication of HIV in a patient with cART, but once integrated into the genome of a T-cell or macrophage the virus gets replicated along with cell's DNA. There have been some clever studies of late that have shown that the persistent virus in patients is coming from the long lived cells replicating, not the virus replicating on its own in a protected niche.

The mechanism of action of BIT225 (on the late expressed vpu protein) is not going to help here. What is needed is better activators of the latent virus. There have been a whole series of preclinical papers published looking at this problem and people have found combinations that seem to work in vitro. I am sure we will start to see new trials using these in the next few years. All great for the patients, but not much help for the shareholders of BIT.