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Viruses hijack a long non-coding RNA

Manipulation of host-cell metabolism is an essential aspect of viral replication cycles. Viral co-option of a cellular long non-protein-coding RNA has now been found to be a key step in this process.
  1. Nicholas S. Heaton

    1. Nicholas S. Heaton is in the Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.

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  2. Bryan R. Cullen

    1. Bryan R. Cullen is in the Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.

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Viruses are totally reliant on the metabolic products of the cells they infect. Indeed, there have been numerous reports of viruses actively modulating cellular metabolism to establish an optimal environment for replication1. Most such studies have found that these metabolic alterations are accomplished by viral targeting of protein–protein interactions, or targeting of host messenger RNAs by virally derived, non-protein-coding microRNAs. Could a class of host RNA known as long non-coding RNAs (lncRNAs) also be targeted to achieve a similar goal? Analysis of the roles of cellular and viral lncRNAs in infection has previously focused mainly on modulation of innate immune responses2. Now, writing in Science, Wang et al.3 reveal a different mechanism by which the virus appropriates host-derived lncRNA: activation of a host-cell metabolic pathway required for viral replication.

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Nature 552, 184-185 (2017)

doi: https://doi.org/10.1038/d41586-017-07692-w

References

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  3. Wang, P., Xu, J., Wang, Y. & Cao, X. Science http://dx.doi.org/10.1126/science.aao0409 (2017).

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