Abstract
Fine-tuning a blunt tool: Regulation of viral host shutoff RNases.
Highlights
We have demonstrated that these spliced influenza messenger RNAs (mRNAs) are still protected from polymerase acidic-X (PA-X) degradation [13], perhaps because their splicing does not require the same factors as host pre-mRNAs or because splicing of viral transcripts is inefficient
The nuclear fraction of these proteins is likely used for a separate function of these enzymes in viral DNA processing [6,44] (Fig 1C). Because this genome processing function is conserved in all herpesviruses, including alpha-herpesviruses like HSVs [3,6,7,44], it appears that in alpha-herpesviruses, host shutoff and genome processing are separated by both localization and active factor, whereas in gamma-herpesviruses localization is the key determinant
Host shutoff is a key feature of many viral replication cycles that profoundly alters the host gene expression profile
Summary
Viral host shutoff RNases include the influenza A virus polymerase acidic-X (PA-X) [1], the herpes simplex viruses (HSV-1 and -2) virion host shutoff protein (vhs) [2], and the Kaposi’s sarcoma-associated herpesvirus (KSHV) shutoff and exonuclease (SOX) protein [3] and its homologs, muSOX from murine gammaherpesvirus 68 (MHV68) [4] and BGLF5 from Epstein–Barr virus (EBV) [5]. The SRE appears to protect mRNAs from degradation by PA-X and vhs, as well as the SOX homologs [31] Overall, these studies show that host shutoff RNases have multiple levels of RNA selectivity that counteracts the apparent promiscuity of these enzymes
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