PerspectiveMolecular Biology

Viruses hijack a host lncRNA to replicate

See allHide authors and affiliations

Science  24 Nov 2017:
Vol. 358, Issue 6366, pp. 993-994
DOI: 10.1126/science.aar2300

You are currently viewing the summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Summary

Viruses are parasitic entities that lack the basic metabolic machinery required to provide the energy and biosynthetic building blocks needed for their replication. To overcome this obstacle, viruses hijack the cellular metabolic machinery of their hosts in order to complete their life cycle and propagate. Yet, how viruses rewire cellular metabolic pathways remains poorly understood. On page 1051 of this issue, Wang et al. (1) identify a long noncoding RNA (lncRNA) called lncRNA-ACOD1 that is potently induced by multiple viruses, including vesicular stomatitis virus, vaccinia virus, and herpes simplex virus 1, in several mouse tissues, as well as by influenza virus in several human cell lines. This lncRNA promotes viral replication through the activation of the metabolic enzyme glutamic-oxaloacetic transaminase 2 (GOT2). Importantly, as enhancement of GOT2 activity by lncRNA-ACOD1 is required for optimal viral replication, mouse and human cells are dramatically protected from infection by simply down-regulating the amounts of this single lncRNA. Thus, this work uncovers a critical evolutionarily conserved mechanism by which viruses co-opt cellular metabolism for their own benefit. Moreover, it unveils a previously uncharacterized function of lncRNAs that could potentially be exploited for the development of new antiviral therapeutics.