What finding would most likely indicate the effectiveness of a new protease inhibitor in HIV replication?

The finding that would most likely indicate the effectiveness of a new protease inhibitor in HIV replication is the lack of a mature core. Protease inhibitors work by disrupting the proteolytic processing of viral polyproteins, which is crucial for the maturation of the virus. HIV-1 relies on the viral protease to cleave its polyprotein precursors into functional proteins, including structural proteins necessary for creating a mature viral particle.

When a protease inhibitor is effective, the cleavage process is inhibited, leading to the production of immature viral particles. These immature particles lack a proper core structure and are unable to infect new cells effectively, as they fail to contain the fully processed proteins necessary for infectivity and replication. Observing a lack of mature cores would thus be a clear indicator that the protease inhibitor is functioning as intended, preventing the virus from maturing and hence limiting its ability to propagate.

Other options, while related to various stages of the HIV life cycle, do not specifically connect to the action of protease inhibitors. For example, integration of proviral DNA into the host genome and transcription from the HIV promoter indicate successful steps in the HIV replication process. The binding of the virus to CD4 is an initial step in the infection of host cells