Interferon-inducible TRIM22 contributes to maintenance of HIV-1 proviral latency in T cell lines

Filippo Turrini, Fabio Saliu, Greta Forlani, Atze T. Das, Carine Van Lint, Roberto S. Accolla, Ben Berkhout, Guido Poli, Elisa Vicenzi

Research output: Contribution to journalArticlepeer-review


The human immunodeficiency virus type-1 (HIV-1) establishes a state of latent infection in a small number of CD4+ T lymphocytes that, nonetheless, represent a major obstacle to viral eradication. We here show that Tripartite Motif-containing protein 22 (TRIM22), an epigenetic inhibitor of Specificity protein 1 (Sp1)-dependent HIV-1 transcription, is a relevant factor in maintaining a state of repressed HIV-1 expression at least in CD4+ T cell lines. By knocking-down (KD) TRIM22 expression, we observed an accelerated reactivation of a doxycycline (Dox)-controlled HIV-1 replication in the T lymphocytic SupT1 cell line. Furthermore, we here report for the first time that TRIM22 is a crucial factor for maintaining a state of HIV-1 quiescence in chronically infected ACH2 -T cell line while its KD potentiated HIV-1 expression in both ACH-2 and J-Lat 10.6 cell lines upon cell stimulation with either tumor necrosis factor-α (TNF-α) or histone deacetylase inhibitors (HDACi). In conclusion, TRIM22 is a novel determinant of HIV-1 latency, at least in T cell lines, thus representing a potential pharmacological target for strategies aiming at curtailing or silencing the pool of latently infected CD4+ T lymphocytes constituting the HIV-1 reservoir in individuals receiving combination antiretroviral therapy.

Original languageEnglish
Article number197631
JournalVirus Research
Publication statusPublished - Aug 2019


  • CD4T cell lines
  • HIV-1 latency
  • Latency-reversing agents
  • Sp1
  • TRIM22

ASJC Scopus subject areas

  • Cancer Research
  • Virology
  • Infectious Diseases


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