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Duplication and divergence of the retrovirus restriction gene Fv1 in Mus caroli allows protection from multiple

Melvyn W Yap1, George R Young1, Renata Varnaite1

  • 1The Francis Crick Institute, London, United Kingdom.

Plos Genetics
|June 12, 2020
PubMed

Insights

Wild mice possess diverse Fv1 and Fv7 genes that act as antiviral defenses. Gene duplication and natural selection drive the evolution of these host restriction factors against various retroviruses.

Area of Science:

  • Evolutionary biology
  • Virology
  • Genetics

Background:

  • Host-pathogen interactions involve an evolutionary arms race.
  • Cell-autonomous restriction factors, such as Fv1, are key host defenses.
  • Fv1 restricts murine leukemia virus (MLV) in laboratory mice, and related factors in wild mice show broader antiviral activity.

Purpose of the Study:

  • To investigate the diversity and antiviral activity of Fv1 genes in wild mice from Thailand.
  • To characterize a newly identified Fv1 gene copy, Fv7, and its evolutionary origins.
  • To understand the role of gene duplication and natural selection in the evolution of host antiviral defenses.

Main Methods:

  • Surveyed Fv1 genes in wild mouse populations in Thailand.
  • Characterized restriction activities against a panel of retroviruses.
  • Analyzed gene duplication events, positive selection, and sequence variations (insertions/deletions).

Main Results:

  • Identified an extra Fv1 gene copy, Fv7, in Mus caroli, M. cervicolor, and M. cookii, likely arising from LINE-mediated retroduplication.
  • Observed significant natural variation in Fv1 and Fv7 genes, including length-altering insertions and deletions.
  • Demonstrated a range of restriction phenotypes against gamma-, spuma-, and lentiviruses.
  • Evidence of positive selection acting on specific residues within Fv1 and Fv7 genes.

Conclusions:

  • Gene duplication, as seen with Fv7, can expand the antiviral restriction repertoire of a host species.
  • Viral pressure, particularly from gamma-, spuma-, and lentiviruses, likely drives the ongoing evolution of Fv1 and Fv7 genes.
  • These findings highlight the dynamic interplay between host genetic variation and viral evolution in natural populations.

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