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Emerging translation strategies during virus–host interaction

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Abstract Translation control is crucial during virus–host interaction. On one hand, viruses completely rely on the protein synthesis machinery of host cells to propagate and have evolved various mechanisms to redirect the host's ribosomes toward their viral mRNAs. On the other hand, the host rewires its translation program in an attempt to contain and suppress the virus early on during infection; the antiviral program includes specific control on protein synthesis to translate several antiviral mRNAs involved in quenching the infection. As the infection progresses, host translation is in turn inhibited in order to limit viral propagation. We have learnt of very diverse strategies that both parties utilize to gain or retain control over the protein synthesis machinery. Yet novel strategies continue to be discovered, attesting for the importance of mRNA translation in virus–host interaction. This review focuses on recently described translation strategies employed by both hosts and viruses. These discoveries provide additional pieces in the understanding of the complex virus–host translation landscape. This article is categorized under: Translation > Translation Mechanisms Translation > Translation Regulation
Emerging mechanisms of translation control during viral infection. (A) Transcription of viral mRNAs and alteration of the tRNA pools during the antiviral state impact translation. Viral mRNAs often possess dissimilar codon usage than that of host mRNAs, consequently altering the tRNA pools by their unique consumption of tRNAs. The antiviral state also changes the composition of the tRNA pools. Ultimately, such altered tRNA pools might affect the elongation rate of a defined subset of mRNAs. (B) tRNA fragments impair translation during viral infection. tRNA fragments abundance increases in infected cells. These fragments might in turn inhibit translation via their interaction with translating ribosomes or via the RNA interference machinery. (C) m6A is a layer of translation control in virus–host interaction. m6A machinery is activated during infection. m6A might enhance or disrupt translation depending on the effector proteins
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Various scenarios of stalled elongation. (a) Normal elongating ribosomes. (b) Ribosome stalling due to depletion of certain amino acids or tRNAs. (c) Suboptimal codon usage that requires rare tRNAs for decoding may also cause ribosome stalling. (d) Certain amino acid motifs, such as di‐proline (XPPX) depicted here, can also cause ribosome stalling
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Translation > Translation Mechanisms

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