Peter Svensson

I am a Principal Researcher and Associate Professor (Docent) in Functional Genomics at the Department of Medicine Huddinge, Karolinska Institutet. I lead an independent research group focused on the epigenetic and chromatin-based mechanisms that govern HIV-1 transcription, latency, and the maintenance of the viral reservoir — with the long-term goal of contributing to a functional cure for HIV.

I completed my Ph.D. in 2006 at Leiden University Medical Center (The Netherlands) and Uppsala University (Sweden). I then undertook postdoctoral training in the laboratory of Leona Samson at the Massachusetts Institute of Technology (MIT). In 2010, I established my research group at Karolinska Institutet. Between 2015 and 2017, I was a Visiting Scientist at the Gladstone Institute of Virology and Immunology in San Francisco. My research has been carried out in close collaboration with clinical HIV researchers and international partners, reflecting a commitment to translational impact.

HIV-1 infection remains one of the most significant challenges in global health. Although current antiretroviral therapy is highly effective at suppressing viral replication and has transformed HIV into a manageable chronic condition, it does not eliminate the provirus in infected cells. The fundamental obstacle to a cure is the persistence of a latent viral reservoir: cells in which the HIV-1 genome is integrated as a provirus but remains transcriptionally silent, invisible to the immune system and insensitive to antiviral drugs. When therapy is interrupted, this reservoir will almost inevitably reseed the infection.

The research group investigates how chromatin structure and epigenetic mechanisms control HIV-1 transcription and the transition between active replication and latency. We are particularly interested in the fate of the HIV-1 provirus in the stably infected primary CD4+ T cells. A central finding of our work is that latent proviruses are not epigenetically uniform: proviruses embedded within heterochromatin are highly refractory to reactivation, while proviruses carrying enhancer-like chromatin features are readily induced. This distinction has important implications for understanding which infected cells drive viral activity/rebound and how the reservoir is maintained over time.

More recently, we have extended our focus to include genome-wide characterization of the HIV-1 reservoir using functional chromatin profiling approaches. We have identified a role for the enzyme PADI4 and histone H3 citrullination in regulating proviral states. Our studies aim to provide mechanistic insights that can inform the rational design of cure-oriented strategies, including approaches to selectively reactivate and eliminate the latent reservoir, or to reinforce silencing to achieve durable remission.

Course director for MTLS Degree project in Molecular Life Science (5MT016)

Teaching in Genetics, Genomics and Functional Genomics (1BI050), Biomedical Research Literacy (4BI134), Epigenetics and its Clinical Applications (2601), Human Viral Diseases: Mechanisms and Pathogenesis.