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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

A role for cytoplasmic PML in cellular resistance to viral infection

Beth A McNally1, Joanne Trgovcich, Gerd G Maul

  • 1Division of Cancer Immunology, Department of Pathology, The Ohio State University Medical Center, Columbus, Ohio, United States of America.

Plos One
|May 30, 2008
PubMed

Insights

Cytoplasmic promyelocytic leukemia (PML) isoforms, specifically PML Ib, defend against herpes simplex virus-1 (HSV-1) by sequestering viral protein ICP0. This finding reinterprets PML

Area of Science:

  • Molecular Biology
  • Virology
  • Cellular Biology

Background:

  • The PML gene, known for its role in acute promyelocytic leukemia (APL) via t(15:17) translocation with retinoic acid receptor (RAR) alpha, encodes a nuclear protein involved in diverse cellular processes.
  • Nuclear PML protein is implicated in cell growth, tumor suppression, apoptosis, transcriptional regulation, chromatin remodeling, DNA repair, and anti-viral defense.
  • PML protein localization dramatically changes during viral infections, traditionally considered a viral mechanism to enhance replication.

Purpose of the Study:

  • To investigate the role of specific promyelocytic leukemia (PML) splice variants during viral infection.
  • To determine if cytoplasmic PML isoforms contribute to intrinsic cellular defense against herpes simplex virus-1 (HSV-1).
  • To elucidate the mechanism by which PML influences HSV-1 infection, focusing on the interaction with viral protein ICP0.

Main Methods:

  • Analysis of PML protein localization and expression patterns in cells exposed to HSV-1.
  • Identification and characterization of specific PML splice variants, particularly those lacking exons 5 & 6.
  • Investigation of the interaction between cytoplasmic PML isoforms and HSV-1 infected cell protein (ICP) 0.

Main Results:

  • A subset of cytoplasmic PML isoforms, lacking exons 5 & 6, are enriched in cells infected with HSV-1.
  • The PML isoform PML Ib, which lacks exons 5 & 6, demonstrates a role in intrinsic cellular defense against HSV-1.
  • PML Ib mediates this defense by sequestering the HSV-1 protein ICP0 within the cytoplasm.

Conclusions:

  • Cytoplasmic PML, particularly the PML Ib isoform, plays a crucial role in the innate immune response against HSV-1.
  • The cytoplasmic sequestration of viral ICP0 by PML Ib is a key mechanism of this anti-viral defense.
  • The observed redistribution of PML in infected cells may represent an active cellular defense strategy, not solely a viral manipulation.

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