Unintegrated HIV-1 DNA recruits cGAS via its histone-binding domain to escape innate immunity
To ensure optimal replication and spread, viruses have evolved countermeasures to evade type 1 IFN-mediated antiviral activity. During the early viral replication cycle steps until uncoating, the HIV-1 core protects viral pathogen associated molecular patterns (viral RNA and reverse transcription products) from recognition by innate immune sensors, including cGAS. However, after capsid uncoating, unintegrated viral DNA (uvDNA) becomes accessible. Here, we show that HIV-1 uses chromatin-mediated cGAS inactivation as a mechanism to protect its uvDNA from innate immune activation.
Authors
- Lucie Bonnet‐Madin
- Monsef Benkirane (ORCID: https://orcid.org/0000-0002-8286-4405)
- Suzie Thenin-Houssier (ORCID: https://orcid.org/0000-0001-7713-9391)
- Cyprien Jahan
- Bijan Sobhian (ORCID: https://orcid.org/0000-0001-7255-6006)
- Shinichi Machida (ORCID: https://orcid.org/0009-0002-8891-4888)
Institutions
- Centre National de la Recherche Scientifique (FR)
- Université de Montpellier (FR)
- National Center for Global Health and Medicine (JP)
- Institut de Génétique Moléculaire de Montpellier (FR)
- Center for Global Health (US)
Publication Details
- Journal
- Proceedings of the National Academy of Sciences
- Published
- 2025-03-11
- DOI
- https://doi.org/10.1073/pnas.2424465122
- Citations
- 5
- Primary Topic
- HIV Research and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 5.18
Funders
- Styrelsen för Internationellt Utvecklingssamarbete
- Gilead Sciences
- Agence Nationale de Recherches sur le Sida et les Hépatites Virales
- Kato Memorial Bioscience Foundation
- European Research Council
- Japan Society for the Promotion of Science