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ISG15 deficiency restricts HIV-1 infection.

Denise Jurczyszak1,2,3,4,5,6, Lara Manganaro7,8, Sofija Buta1,2,3,4,5,6

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Individuals lacking interferon stimulated gene 15 (ISG15) show enhanced resistance to HIV-1 infection. This resistance is linked to elevated interferon stimulated genes (ISGs) and impacts viral replication at multiple stages.

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Type I interferons (IFN-Is) are crucial cytokines that induce interferon stimulated genes (ISGs).
  • ISG15 is a key regulator of the IFN-I signaling pathway and viral resistance.
  • ISG15 deficiency leads to elevated ISGs and broad-spectrum viral resistance.

Purpose of the Study:

  • To investigate the role of ISG15 in HIV-1 infection.
  • To determine if ISG15 deficiency confers resistance to HIV-1.
  • To identify the mechanisms underlying ISG15-mediated antiviral activity against HIV-1.

Main Methods:

  • Fibroblast and primary CD4+ T cell cultures from ISG15-deficient and control individuals.
  • Infection assays with single-cycle HIV-1.
  • Complementation studies with wild-type ISG15 and ISG15ΔGG.
  • CRISPR-Cas9 gene editing to create ISG15 knockout (ISG15ko) cells.
  • Transcriptome analysis (RNA sequencing).

Main Results:

  • ISG15-deficient fibroblasts showed increased resistance to HIV-1 infection compared to controls.
  • Complementation with ISG15 restored HIV-1 susceptibility.
  • CRISPR-edited ISG15ko CD4+ T cells were less susceptible to HIV-1 infection.
  • Transcriptome analysis revealed ISG signatures in ISG15ko cells, similar to ISG15-deficient patients.

Conclusions:

  • ISG15 deficiency confers resistance to HIV-1 infection.
  • This resistance is mediated by ISG-induced antiviral mechanisms targeting HIV-1 at multiple replication steps.
  • Both known and unknown ISGs contribute to the antiviral state in ISG15-deficient cells.