Sindbis virus usurps the cellular HuR protein to stabilize its transcripts and promote productive infections in mammalian and mosquito cells.

How viral transcripts are protected from the cellular RNA decay machinery and the importance of this protection for the virus are largely unknown. We demonstrate that Sindbis virus, a prototypical single-stranded arthropod-borne alphavirus, uses U-rich 3' UTR sequences in its RNAs to recruit a known regulator of cellular mRNA stability, the HuR protein, during infections of both human and vector mosquito cells. HuR binds viral RNAs with high specificity and affinity.

Virus-mediated mRNA decay by hyperadenylation.

Degradation of cellular mRNAs during Kaposi's sarcoma-associated herpesvirus infection is associated with hyperadenylation of transcripts and a relocalization of cytoplasmic poly(A)-binding proteins to the nucleus.