It has been hypothesized that eIF3d is cleaved upon viral infection by PR present in incoming virions, possibly explaining an earlier study in which 1 h pre-treatment of H9 cells with a HIV-1 PR inhibitor (UK-88947) strongly inhibited HIV-1 DNA synthesis 18 h post-infection, thus suggesting the requirement of HIV-1 PR for optimal viral genome RT processing and integration [61]. The gene discussed is EIF3D; the disease is viral infectious disease.