Common position of indels that cause deviations from canonical genome organization in different measles virus strains

Jelena Ivancic-Jelecki1,2, Anamarija Slovic3,4, Maja Šantak3,4

  • 1University of Zagreb, Centre for research and knowledge transfer in biotechnology, Rockefellerova 10, 10 000, Zagreb, Croatia. jivancic@unizg.hr.

Virology Journal
|July 31, 2016
PubMed
Abstract

Insights

Researchers identified a specific genomic region in measles virus (MV) that may correct genome length after mutations occur. This finding sheds light on MV genome stability and replication mechanisms.

Area of Science:

  • Virology
  • Genomics
  • Molecular Biology

Background:

  • The measles virus (MV) typically has a fixed genome size of 15,894 nucleotides.
  • Deviations from this canonical genome organization, such as insertions or deletions (indels), are rare and often involve compensatory mutations to maintain genome length.
  • While programmed nucleotide additions occur during transcription, a similar mechanism for non-random genome length correction after replication indels has not been described for the complete MV genome.

Purpose of the Study:

  • To investigate whether measles virus strains with non-canonical genome organizations share common genetic characteristics.
  • To explore potential mechanisms for non-random genome length correction in measles virus.

Main Methods:

  • Compilation of 64 complete measles virus (MV) genomic sequences from open-access databases.
  • Performance of multiple sequence comparisons and phylogenetic analyses.
  • Identification and characterization of deviations from canonical genome organization in MV sequences.

Main Results:

  • Deviations from canonical MV genome organization were detected in 11 sequences due to short indels.
  • In nine of these, a common mutation (insertion or deletion) was found in a specific 28-nucleotide region within the F gene 5' untranslated region.
  • This region, characterized by homopolymeric stretches, maintained a total length of 28 nucleotides in canonical strains despite variations in individual repeat lengths.

Conclusions:

  • A specific, conserved genomic region in MV appears to be mutated across unrelated wild-type strains.
  • This suggests a potential role for this region in non-random genome length corrections during MV replication.
  • Further research is needed to elucidate the precise mechanism of this correction.

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