ArticleNucleic acids research2020
HIV-1 infection activates endogenous retroviral promoters regulating antiviral gene expression.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
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- Interactions between human immunodeficiency virus and human endogenous retroviruses.Journal of virology · 2025Review
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- Viral influencers: deciphering the role of endogenous retroviral LTR12 repeats in cellular gene expression.Journal of virology · 2025Review
- Reactivation of latent HIV-1 by the glucocorticoid receptor modulator AZD9567.Journal of virology · 2025Article
- Transposable elements may enhance antiviral resistance in HIV-1 elite controllers.Genome biology · 2025Article
- HERV-K10 as a mediator of immune modulation in hepatitis infections.Frontiers in immunology · 2025Article
- From mechanisms to therapies: the multifaceted roles of guanylate-binding protein 2 in immunity, cancer, and beyond.Frontiers in immunology · 2025Review
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Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although endogenous retroviruses (ERVs) are known to harbor cis-regulatory elements, their role in modulating cellular immune responses remains poorly understood. Using an RNA-seq approach, we show that several members of the ERV9 lineage, particularly LTR12C elements, are activated upon HIV-1 infection of primary CD4+ T cells. Intriguingly, HIV-1-induced ERVs harboring transcription start sites are primarily found in the vicinity of immunity genes. For example, HIV-1 infection activates LTR12C elements upstream of the interferon-inducible genes GBP2 and GBP5 that encode for broad-spectrum antiviral factors. Reporter assays demonstrated that these LTR12C elements drive gene expression in primary CD4+ T cells. In line with this, HIV-1 infection triggered the expression of a unique GBP2 transcript variant by activating a cryptic transcription start site within LTR12C. Furthermore, stimulation with HIV-1-induced cytokines increased GBP2 and GBP5 expression in human cells, but not in macaque cells that naturally lack the GBP5 gene and the LTR12C element upstream of GBP2. Finally, our findings suggest that GBP2 and GBP5 have already been active against ancient viral pathogens as they suppress the maturation of the extinct retrovirus HERV-K (HML-2). In summary, our findings uncover how human cells can exploit remnants of once-infectious retroviruses to regulate antiviral gene expression.
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