Editorial
SERINC5: not all splice variants work against HIV
Abstract
The battle between viruses and their host is armed by cellular defences, often referred to as restriction factors, on one side, and by the counteracting measures expressed by viral genomes, on the other side. The presence of cell-derived barriers which interfere with virus replication was first revealed for retroviruses in the 70s. Since the description of FV1 (1), a cytoplasmic murine factor inhibiting MLV replication, several blocks that impair replication of viruses on the cell surface, in the cytoplasm, and in the nucleus have later been discovered. The latest addition to the list is SERINC5, a cellular protein which was recently found to block retrovirus delivery into target cells (2,3).