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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

Viral attachment induces rapid recruitment of an innate immune sensor (TRIM5α) to the plasma membrane

Seiga Ohmine1, Raman Deep Singh, David L Marks

  • 1Department of Molecular Medicine, Mayo Clinic, Rochester, MN 55905, USA.

Journal of Innate Immunity
|April 4, 2013
PubMed

Insights

Tripartite motif 5 alpha (TRIM5α) rapidly moves to the cell membrane upon encountering HIV-1, enhancing its ability to block viral infection. This TRIM5α recruitment is crucial for innate immune sensing and restricting retroviral entry.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • TRIM5α functions as a pattern recognition receptor targeting retroviral capsids.
  • It blocks human immunodeficiency virus type 1 (HIV-1) infection post-entry.
  • The exact mechanisms of TRIM5α's rapid viral recognition are not fully understood.

Purpose of the Study:

  • To investigate how viral exposure influences TRIM5α localization and function.
  • To elucidate the role of TRIM5α recruitment to the plasma membrane in innate immune sensing.
  • To understand TRIM5α's mechanism in restricting retroviral infection.

Main Methods:

  • Total internal reflection fluorescence microscopy to observe TRIM5α dynamics.
  • Lipid flotation assays to analyze TRIM5α association with membrane microdomains.
  • Utilized HIV-1 viral-like particles (VLPs) and HIV-1 vectors for stimulation.
  • Investigated endogenous TRIM5α translocation in human T cells.

Main Results:

  • TRIM5α rapidly localized to the plasma membrane (PM) upon exposure to HIV-1 VLPs, but not Env-less VLPs.
  • TRIM5α signals colocalized with HIV-1 capsid at the PM.
  • HIV-1 Env-pseudotyped vectors induced TRIM5α translocation to lipid microdomains.
  • Clustering of lipid microdomains also triggered TRIM5α recruitment to the PM.
  • Prior TRIM5α recruitment enhanced restriction potency against HIV-1.

Conclusions:

  • TRIM5α recruitment to the PM is triggered by specific viral components, particularly the HIV-1 capsid.
  • This PM localization is essential for TRIM5α-mediated innate immune sensing.
  • TRIM5α's translocation to lipid microdomains and subsequent PM recruitment are key steps in restricting retroviral infection.

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