ArticlePLoS pathogens2020
Genome-wide CRISPR knockout screen identifies ZNF304 as a silencer of HIV transcription that promotes viral latency.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Identification of Endometriosis Pathophysiologic-Related Genes Based on Meta-Analysis and Bayesian Approach.International journal of molecular sciences · 2025Pooled it
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- Extracellular condensates (ECs) are endogenous modulators of HIV transcription and latency reactivation.Molecular psychiatry · 2026Article
- PIM1 and PIM3 Kinases Suppress HIV-1 Protein Expression and Particle Production Through Distinct Roles.Pathogens (Basel, Switzerland) · 2026Article
- Epigenetic mechanisms of retroviral regulation: a comparative review.Epigenetics & chromatin · 2026Review
- CBX8 suppresses autophagy-dependent senescence in colorectal cancer by modulating the mTOR signaling pathway.International journal of biological sciences · 2026Article
- Engineering non-pathogenic bacteria for auto-transporter-driven secretion of functional interferon.Gut microbes · 2025Article
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- HIV-1 latency: From acquaintance to confidant.Journal of virus eradication · 2025Review
- CRISPR editing of candidate host factors that impact influenza A virus infection.Microbiology spectrum · 2025Article
- Interleukin-27-polarized HIV-resistant M2 macrophages are a novel subtype of macrophages that express distinct antiviral gene profiles in individual cells: implication for the antiviral effect via different mechanisms in the individual cell-dependent manner.Frontiers in immunology · 2025Article
- Manganese mediates antiviral effects by driving an ATM -TBK1 phosphorylation signaling pathway.Frontiers in immunology · 2025Article
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- KAP1/TRIM28 - antiviral and proviral protagonist of herpesvirus biology.Trends in microbiology · 2024Article
- Review
- Secretion of functional interferon by the type 3 secretion system of enteropathogenic Escherichia coli.Microbial cell factories · 2024Article
- Direct and indirect effects of CYTOR lncRNA regulate HIV gene expression.PLoS pathogens · 2024Article
- Review
- ZNF283, a Krüppel-associated box zinc finger protein, inhibits RNA synthesis of porcine reproductive and respiratory syndrome virus by interacting with Nsp9 and Nsp10.Veterinary research · 2024Article
- Identification of PANoptosis-Related Genes in Community-Acquired Pneumonia Diagnosis.Journal of inflammation research · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the widespread use of anti-retroviral therapy, human immunodeficiency virus (HIV) still persists in an infected cell reservoir that harbors transcriptionally silent yet replication-competent proviruses. While significant progress has been made in understanding how the HIV reservoir is established, transcription repression mechanisms that are enforced on the integrated viral promoter have not been fully revealed. In this study, we performed a whole-genome CRISPR knockout screen in HIV infected T cells to identify host genes that potentially promote HIV latency. Of several top candidates, the KRAB-containing zinc finger protein, ZNF304, was identified as the top hit. ZNF304 silences HIV gene transcription through associating with TRIM28 and recruiting to the viral promoter heterochromatin-inducing methyltransferases, including the polycomb repression complex (PRC) and SETB1. Depletion of ZNF304 expression reduced levels of H3K9me3, H3K27me3 and H2AK119ub repressive histone marks on the HIV promoter as well as SETB1 and TRIM28, ultimately enhancing HIV gene transcription. Significantly, ZNF304 also promoted HIV latency, as its depletion delayed the entry of HIV infected cells into latency. In primary CD4+ cells, ectopic expression of ZNF304 silenced viral transcription. We conclude that by associating with TRIM28 and recruiting host transcriptional repressive complexes, SETB1 and PRC, to the HIV promoter, ZNF304 silences HIV gene transcription and promotes viral latency.
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