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Promyelocytic leukemia protein is a restriction factor for Junín virus independently of Z matrix protein

Federico Giovannoni1, Cecilia A Vazquez1, Pablo Thomas2

  • 1Laboratorio de Estrategias Antivirales, Instituto de Química Biológica, Facultad de Ciencias Exactas y Naturales, IQUIBICEN, UBA-CONICET, Buenos Aires, Argentina.

Biochemical and Biophysical Research Communications
|April 1, 2022
PubMed

Insights

Junín virus (JUNV) restricts Promyelocytic leukemia protein (PML) in human cells, unlike LCMV. JUNV infection increases PML expression, showing a distinct interaction with this antiviral factor.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Promyelocytic leukemia protein (PML) acts as a viral restriction factor, but its mechanisms vary.
  • Previous studies linked Old World mammarenavirus LCMV infection to PML nuclear-cytoplasmic translocation mediated by the Z protein.

Purpose of the Study:

  • To investigate the interaction between the New World mammarenavirus Junín virus (JUNV) and PML.
  • To determine if JUNV infection induces PML translocation, contrasting with LCMV behavior.

Main Methods:

  • JUNV infection of human A549 cells.
  • Analysis of PML expression levels.
  • Assessment of PML localization and colocalization with JUNV Z protein.

Main Results:

  • PML restricts JUNV infection in human A549 cells.
  • JUNV infection leads to enhanced PML expression.
  • Unlike LCMV, JUNV infection does not cause PML translocation to the cytoplasm.
  • PML does not colocalize with JUNV Z protein.

Conclusions:

  • Junín virus (JUNV) interacts differently with the antiviral protein PML compared to lymphocytic choriomeningitis virus (LCMV).
  • JUNV evades PML-mediated restriction through a mechanism that does not involve PML translocation.
Keywords:
Junín virusMammarenavirusPromyelocytic leukemia proteinRestriction factor

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