The universal bacterial transcription elongation factor NusA mediates elongation activities of RNA polymerase. By itself, NusA induces transcription pausing and facilitates intrinsic termination, but NusA also is a cofactor of antiterminators that antagonize pausing and prevent termination. We show that NusA is required for λ-related phage 82 antiterminator Q 82 to construct a stable complex in which RNA-based termination mechanisms have restricted access to the emerging transcript; this result suggests a locale for both Q 82 and NusA near the β flap domain of RNA polymerase. Furthermore, as NusA is not required for the antipausing activity of Q 82 in vitro, we distinguish two distinct activities of antiterminators, namely antipausing and RNA occlusion, and discuss their roles in Q 82 function.