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Fatal attraction: The roles of ribosomal proteins in the viral life cycle

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Abstract Upon viral infection of a host cell, each virus starts a program to generate many progeny viruses. Although viruses interact with the host cell in numerous ways, one critical step in the virus life cycle is the expression of viral proteins, which are synthesized by the host ribosomes in conjunction with host translation factors. Here we review different mechanisms viruses have evolved to effectively seize host cell ribosomes, the roles of specific ribosomal proteins and their posttranslational modifications on viral RNA translation, or the cellular response to infection. We further highlight ribosomal proteins with extra‐ribosomal function during viral infection and put the knowledge of ribosomal proteins during viral infection into the larger context of ribosome‐related diseases, known as ribosomopathies. This article is categorized under: Translation > Translation Mechanisms Translation > Translation Regulation
Canonical cap‐dependent translation requires a m7G‐capped mRNA and the eIF4F complex (eIF4E, eIF4A, and eIF4G) . A large group of viruses does not contain a cap and instead uses an internal ribosome entry sites (IRES) and a subset of translation factors for initiation
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The binding of a ribosomal protein with extra‐ribosomal function to a viral protein can either neutralize it and block virus proliferation, or it can help to activate cellular or viral pathways and functions to promote virus proliferation
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The PTM status of certain ribosomal proteins is altered in response to viral infection. Ribosomal proteins have been found to largely become phosphorylated, but changes in methylations and acetylations have also been reported
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Front and back view of the human 80S ribosome highlighting ribosomal proteins directly targeted by viruses to facilitate translation of viral mRNAs. Human ribosome adapted from PDB 5T2C (X. Zhang et al., 2016)
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