The physiological significance of eIF3d cleavage might extend from the cap-dependent host cell translation shut-off described above, since its knockdown boosted infectivity upon single round infection with VSV-G pseudotyped HIV-1 particles and promoted accumulation of reverse transcription products [44], thus suggesting an antiviral role for eIF3d during the early stages of viral infection, before proviral integration (Figure 2). The gene discussed is EIF3D; the disease is viral infectious disease.