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Trim69 is a microtubule regulator that acts as a pantropic viral inhibitor

Yuxin Song1, Xuan-Nhi Nguyen1, Anuj Kumar1

  • 1Centre International de Recherche en Infectiologie, Université de Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, École Nationale Supérieure de Lyon, Lyon, France.

Proceedings of the National Academy of Sciences of the United States of America
|October 17, 2022
PubMed

Insights

Tripartite motif protein 69 (Trim69) acts as a key antiviral factor in interferon-stimulated myeloid cells. It inhibits viral infections by stabilizing microtubules, revealing the cytoskeleton

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Interferon (IFN) signaling is crucial for innate antiviral immunity.
  • Myeloid cells play a significant role in host defense against viral pathogens.
  • The specific mechanisms by which IFN-stimulated genes confer antiviral states are not fully elucidated.

Purpose of the Study:

  • To identify novel regulators of viral infection in myeloid cells.
  • To characterize the antiviral function and mechanism of tripartite motif protein 69 (Trim69).
  • To investigate the role of the cytoskeleton in innate antiviral responses.

Main Methods:

  • Functional and evolutionary screening of antiviral factors.
  • In vitro infection assays with various viruses (HIV-1, HIV-2, SIVMAC, VSV, SARS-CoV-2).
  • Co-immunoprecipitation and immunofluorescence to study protein-microtubule interactions.

Main Results:

  • Tripartite motif protein 69 (Trim69) was identified as a negative regulator of viral infection.
  • Trim69 inhibits the early stages of infection for retroviruses and RNA viruses in myeloid cells.
  • Trim69 directly binds to microtubules and promotes their stabilization, a key component of the antiviral response.

Conclusions:

  • Trim69 is an important antiviral innate defense factor.
  • Microtubule stabilization is an integral part of the antiviral response mediated by IFN-I in myeloid cells.
  • The cytoskeleton represents a critical, yet underappreciated, target in host-pathogen interactions during viral infections.
Keywords:
HIVSARS-CoV2innate responseinterferonvirus

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