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No two strands are alike: New mechanism for elongation of viral genome termini

Date:
June 24, 2011
Source:
Albert-Ludwigs-Universität Freiburg
Summary:
Like bacteria, viruses have their own genome. The ends or termini of a viral RNA are especially interesting for virologists because they play an important role in reproduction and in the reaction of the innate immune system to the virus. The genetic information is reproduced when a strand of the genome is transcribed into a complementary strand of the so-called antigenome. This strand then serves as the model or template for the synthesis of a new genome.
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The Borna disease virus has four additional nucleotides each in the genome and antigenome at their 3’ termini.
Credit: Image courtesy of Albert-Ludwigs-Universität Freiburg

Like bacteria, viruses have their own genome. The ends or termini of a viral RNA are especially interesting for virologists because they play an important role in reproduction and in the reaction of the innate immune system to the virus. The genetic information is reproduced when a strand of the genome is transcribed into a complementary strand of the so-called antigenome. This strand then serves as the model or template for the synthesis of a new genome.

As a result of this simple copying mechanism, the two strands are normally exact copies of each another. However, this is not the case with the Borna disease virus (BDV), which belongs to the group of negative-strand RNA viruses. When one compares the genome and the antigenome of the BDV, one finds that the two strands possess four additional nucleotides each as components of the RNA at their 3' termini. There is no template on the complementary strand for this elongation, and the process thus cannot be explained with the standard model of reproduction.

In a new study, a Freiburg research group led by Dr. Urs Schneider (now Québec, Canada) at the Institute of Microbiology and Hygiene, Department of Virology, was able to demonstrate that the additional nucleotides are not transcribed from the complementary strand but from a template located within the newly synthesized viral strand.

The study describes the use of internal templates for RNA synthesis for the first time and presents a previously unknown possibility for modifying viral genome termini. The significance of genome elongation for the reproduction and pathogenesis of the BDV is not yet completely clear. However, there are indications that this mechanism serves the dual function of preserving the integrity of the genome termini and making them unidentifiable for the innate immune system. Further experimentation will be necessary to clarify the significance of the "realignment and elongation" mechanism described in the study.

In some animals (e.g., horses), the BDV establishes a terminal infection that can lead to a severe neurological illness, ending in death.


Story Source:

The above post is reprinted from materials provided by Albert-Ludwigs-Universität Freiburg. Note: Materials may be edited for content and length.


Journal Reference:

  1. A. Martin, N. Hoefs, J. Tadewaldt, P. Staeheli, U. Schneider. Genomic RNAs of Borna disease virus are elongated on internal template motifs after realignment of the 3' termini. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1016759108

Cite This Page:

Albert-Ludwigs-Universität Freiburg. "No two strands are alike: New mechanism for elongation of viral genome termini." ScienceDaily. ScienceDaily, 24 June 2011. <www.sciencedaily.com/releases/2011/04/110418083351.htm>.
Albert-Ludwigs-Universität Freiburg. (2011, June 24). No two strands are alike: New mechanism for elongation of viral genome termini. ScienceDaily. Retrieved August 1, 2015 from www.sciencedaily.com/releases/2011/04/110418083351.htm
Albert-Ludwigs-Universität Freiburg. "No two strands are alike: New mechanism for elongation of viral genome termini." ScienceDaily. www.sciencedaily.com/releases/2011/04/110418083351.htm (accessed August 1, 2015).

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