Viruses are fully reliant on the translation machinery of their host cells to produce the polypeptides that are essential for viral replication. Consequently, viruses recruit host ribosomes to translate viral mRNAs, typically using virally encoded functions to seize control of cellular translation factors and the host signalling pathways that regulate their activity. This not only ensures that viral proteins will be produced, but also stifles innate host defences that are aimed at inhibiting the capacity of infected cells for protein synthesis. Remarkably, nearly every step of the translation process can be targeted by virally encoded functions. This Review discusses the diverse strategies that viruses use to subvert host protein synthesis functions and regulate mRNA translation in infected cells.

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Viral subversion of the host protein synthesis machinery.

Ten Strategies of Interferon Evasion by Viruses.

MicroRNA Regulation of RNA Virus Replication and Pathogenesis.

Viruses are obligate intracellular parasites, and their replication requires host cell functions. Although the size, composition, complexity, and functions encoded by their genomes are remarkably diverse, all viruses rely absolutely on the protein synthesis machinery of their host cells. Lacking their own translational apparatus, they must recruit cellular ribosomes in order to translate viral mRNAs and produce the protein products required for their replication. In addition, there are other constraints on viral protein production. Crucially, host innate defenses and stress responses capable of inactivating the translation machinery must be effectively neutralized. Furthermore, the limited coding capacity of the viral genome needs to be used optimally. These demands have resulted in complex interactions between virus and host that exploit ostensibly virus-specific mechanisms and, at the same time, illuminate the functioning of the cellular protein synthesis apparatus.

/pdf/tinkering-with-translation-protein-synthesis-in-virus-4jkutmm7ty.pdf

Tinkering with Translation: Protein Synthesis in Virus-Infected Cells

Cellular microRNAs serve key roles in the post-transcriptional regulation of almost every cellular gene-regulatory pathway, and it therefore is not surprising that viruses have found ways to subvert this process. Several viruses encode microRNAs that directly downregulate the expression of factors of the innate immune system, including proteins involved in promoting apoptosis and recruiting effector cells of the immune system. Viruses have also evolved the ability to downregulate or upregulate the expression of specific cellular miRNAs to enhance their replication. This Review provides an overview of the present knowledge of the complex interactions of viruses with the microRNA machinery of cells.

/pdf/micrornas-as-mediators-of-viral-evasion-of-the-immune-system-3917m8l382.pdf

MicroRNAs as mediators of viral evasion of the immune system.

http://basicmed.med.ncku.edu.tw/admin/up_img/000315-2.pdf

Enterovirus-induced miR-141 contributes to shutoff of host protein translation by targeting the translation initiation factor eIF4E.

Extracellular vesicle DNA (evDNA) acts as a potential mechanism for intercellular communication and possesses an important diagnostic value for multiple diseases. In this study, we have provided the first example that transcription factor determines the sources of evDNA from chromatin DNA. Transcription factor FOXM1 mediates the loading of specific chromatin DNA fragments into extracellular vesicles (EVs). Specifically, certain chromatin DNA fragments are specified by FOXM1 and form LC3-FOXM1-DNA vesicles in cytoplasm during autophagy. Then the cytoplasmic LC3-FOXM1-DNAs are transported to EVs probably through the process of an autophagy-MVB transport. We have confirmed that LC3-FOXM1-DNAs can be absorbed by recipient cells along with the released EVs and certain evDNA fragments integrate into the genome of recipient cells. This discovery provides an understanding for studying the sources and functions of evDNA and helps to expand its application in the future.

/pdf/transcription-factor-determines-the-sources-of-extracellular-12y39zs6.pdf

Hao Wei Cheng

Papers

Enterovirus-induced miR-141 contributes to shutoff of host protein translation by targeting the translation initiation factor eIF4E.

Transcription factor determines the sources of extracellular vesicle DNA