Mechanisms controlling the latent HIV-1 provirus

HIV is incurable due the persistence of latent but replication competent HIV proviruses. Lifelong antiretroviral therapy (ART) stops HIV progression to AIDS with minimal side effects. However, a HIV cure has only been achieved in rare cases with stem cell transplants. Multiple epigenetic mechanisms dictate the chromatin environment at the HIV integration site which in turn dictate HIV transcription and latency. In this thesis I will explore how histone marks, in particular histone citrullination, and the immune system affect HIV transcription and latency.

List of scientific papers

I. Luca Love*, Bianca B Jutte*, Birgitta Lindqvist, Oscar Kieri, Piotr Nowak, J. Peter Svensson. PADI4-mediated citrullination of histone H3 stimulates HIV-1 transcription. bioRxiv. 2024.03.17.583304. *Equal Contribution. Preprint. [Manuscript]
https://doi.org/10.1101/2024.03.17.583304

II. Lindqvist B*, Jźtte BB*, Love L*, Assi W, Roux J, Sšnnerborg A, Tezil T, Verdin E, Svensson JP. T cell stimulation remodels the latently HIV-1 infected cell population by differential activation of proviral chromatin. PLoS Pathogens. 2022;18(6):e1010555. *Equal Contribution.
https://doi.org/10.1371/journal.ppat.1010555

III. Furtado Mil‹o J, Love L, Gourgi G, Derhaschnig L, Svensson JP, Sšnnerborg A, van Domselaar R. Natural killer cells induce HIV-1 latency reversal after treatment with pan-caspase inhibitors. Frontiers in Immunology. 2022;13:1067767.
https://doi.org/10.3389/fimmu.2022.1067767