Cover photograph: Rotavirus viroplasms are membrane-less globular cytosolic inclusions allowing virus genome replication and its packaging in newly synthesized viral cores; these steps are followed by the addition of a second layer of protein to generate double-layered particles. A point mutation in leucine 124 of the core protein VP2 (simian strain SA11) disrupts its interaction with NSP5, the main viroplasm building- block constituent. The VP2 L124A overexpression in rotavirus-infected BSR-T7 cells works as a dominant negative, forming impaired viroplasms and aberrant distribution of the proteins composing them. Shown is the immunofluorescence (at 6 h postinfection) of rotavirus- infected BSR-T7 cells overexpressing VP2 L124A followed by immunostaining for the detection of NSP5 (anti-NSP5; green), NSP3 (anti- NSP3; red), and VP6 (anti-VP6; cyan). Nuclei were stained with 4ʹ,6-diamidino-2-phenylindole (DAPI; blue). (See related article in April 2020, vol. 94 no. 7, e01965-19.) (Copyright © 2020 American Society for Microbiology. All Rights Reserved.)