Abstract
Diverse animal and plant viruses block the re-infection of host cells by the same or highly similar viruses through superinfection exclusion (SIE), a widely observed, yet poorly understood phenomenon. Here we demonstrate that SIE of turnip crinkle virus (TCV) is exclusively determined by p28, one of the two replication proteins encoded by this virus. p28 expressed from a TCV replicon exerts strong SIE to a different TCV replicon. Transiently expressed p28, delivered simultaneously with, or ahead of, a TCV replicon, largely recapitulates this repressive activity. Interestingly, p28-mediated SIE is dramatically enhanced by C-terminally fused epitope tags or fluorescent proteins, but weakened by N-terminal modifications, and it inversely correlates with the ability of p28 to complement the replication of a p28-defective TCV replicon. Strikingly, p28 in SIE-positive cells forms large, mobile punctate inclusions that trans-aggregate a non-coalescing, SIE-defective, yet replication-competent p28 mutant. These results support a model postulating that TCV SIE is caused by the formation of multimeric p28 complexes capable of intercepting fresh p28 monomers translated from superinfector genomes, thereby abolishing superinfector replication. This model could prove to be applicable to other RNA viruses, and offer novel targets for antiviral therapy.
Highlights
IntroductionSuperinfection exclusion (SIE) refers to the ability of a pre-existing virus (the primary invader) to exclude secondary infections by the same or closely related viruses (superinfectors) at cellular and/or organismal levels
Superinfection exclusion (SIE) refers to the ability of a pre-existing virus to exclude secondary infections by the same or closely related viruses at cellular and/or organismal levels
We describe a transformative discovery that self-perpetuating coalescence of a virus-encoded replication protein serves as a novel mechanism for SIE
Summary
Superinfection exclusion (SIE) refers to the ability of a pre-existing virus (the primary invader) to exclude secondary infections by the same or closely related viruses (superinfectors) at cellular and/or organismal levels. Studies using mutants of CTV, plum pox virus, soilborne wheat mosaic virus, and apple latent spherical virus that were labelled with different fluorescent proteins, established that co-introduced variants of the same virus occupy adjacent, yet non-overlapping cell clusters in the same leaves or tissue niches [10,11,12,13]. These studies clearly demonstrated that SIE among closely related plant virus variants likewise exclude each other at the cellular level, drawing strong parallels between SIEs occurring in plant and animal virus infections
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