Extended poly(A) tails are a shared feature of herpesvirus mRNAs

Erik Fuhrmann1,2, Sae Toda1,3, Jonas Leins1

  • 1Institute of Virology, Hannover Medical School, Hannover, Germany.

Insights

Herpesviruses utilize unusually long poly(A) tails on their messenger RNAs (mRNAs) to enhance gene expression. This extended polyadenylation, unlike in other viruses, provides a significant advantage during infection.

Area of Science:

  • Molecular Biology
  • Virology
  • Genomics

Background:

  • Poly(A) tails are crucial for mRNA stability, translation, and regulation.
  • Most cellular and viral mRNAs possess poly(A) tails, but their lengths vary.
  • Herpesviruses are known for complex gene expression strategies.

Purpose of the Study:

  • To investigate poly(A) tail length distribution on viral and cellular mRNAs during various viral infections.
  • To compare poly(A) tail lengths across different virus families, including Herpesviridae.
  • To understand the role of poly(A) tail length in herpesviral gene expression advantage.

Main Methods:

  • Nanopore direct RNA sequencing was employed to analyze poly(A) tail lengths.
  • Comparative analysis of poly(A) tail distributions on cellular and viral mRNAs.
  • Investigation across Herpesviridae, coronavirus, and poxvirus infections.

Main Results:

  • Herpesvirus mRNAs exhibit significantly longer poly(A) tails compared to cellular and other viral mRNAs.
  • Poly(A) tail lengths of coronaviruses and poxviruses are more similar to host mRNAs.
  • Herpesviral noncoding RNAs show varied poly(A) tailing patterns, and individual mRNAs display dynamic tail length changes.
  • Mixed nucleotide content in herpesviral poly(A) tails was insufficient to explain the extended lengths.

Conclusions:

  • Extended poly(A) tails on herpesvirus mRNAs represent a widespread mechanism enhancing viral gene expression.
  • This finding highlights a novel strategy employed by herpesviruses to gain a competitive advantage.
  • Further research is needed to elucidate the uncharacterized regulatory mechanisms governing herpesviral poly(A) tail lengths.

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