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Mechanisms behind HIV-1 latency and rebound - Peter Svensson's group

In the lab we study interactions between viruses and the host cell. By understanding how these interact we hope to gain insights into both cellular processes and the viral replicative cycle. We focus on HIV-1 and HTLV-1 and how they make use of the host chromatin and transcription machinery.

Close-up image of virus and bacteria cells
3d rendering of viruses and human cells. Photo: jijomathai https://stock.adobe.com

HIV infection is a devastating disease affecting 35 million people worldwide. Current anti-retroviral treatment is highly effective and has made the HIV infection chronic. However, despite more effective treatments, the prospects of a cure are distant. We are involved in efforts to eradicate HIV from patients.

The problem for an HIV cure is that, even though the virus particles are eradicated, the infected cells maintain the information of remake the virus. This information is integrated in the host cell as a provirus. The provirus switches between active and inactive states. Thereby, the infected cells evade both the immune system and death associated with massive viral production.

Close-up of chromatin and nucleosomes
Chromatin consists of nucleosomes where DNA (yellow) is wrapped around histones (blue). A single nuclesome is depicted to the right, a string of nucleosomes to the left. Photo: Juan Gärtner (https://stock.adobe.com) Photo: Juan Gärtner

Our research group is interested in the molecular mechanisms behind the epigenetic state reversal of the HIV-1 provirus. The focus of our research group is to investigate the establishment, maintenance and reversal of epigenetic states of the HIV-1 provirus.  This circuitry of HIV-1 latency is modeled and tested in cell lines, as well as primary cells from both HIV- and HIV+ donors. By characterizing the composition of proviral chromatin and how it connects with transcription and viral production, we have identified several new aspects of how the virus evades the host mechanisms of elimination. Recently, we found that the reactivatable portion of the latent reservoir act as an enhancer.

We view epigenetic state reversal of proviral chromatin as a general model to understand the activation and silencing of other loci important for e.g. development and cancer.

Selected Publications

  1. Chromatin maturation of the HIV-1 provirus in primary resting CD4+ T cells.
    Lindqvist B, Svensson Akusjärvi S, Sönnerborg A, Dimitriou M, Svensson JP. Plos Pathogens 2020 Jan;16(1):e1008264
     
  2. Distinct chromatin functional states correlate with HIV latency reactivation in infected primary CD4+ T cells.
    Battivelli E, Dahabieh MS, Abdel-Mohsen M, Svensson JP, Tojal Da Silva I, Cohn LB, et al
    Elife 2018 05;7():
     
  3. The mTOR Complex Controls HIV Latency.
    Besnard E, Hakre S, Kampmann M, Lim HW, Hosmane NN, Martin A, et al
    Cell Host Microbe 2016 Dec;20(6):785-797

More publications

 

Group members

Peter Svensson

Group leader

Possibilities for students

Motivated students are welcome to do short or longer project degrees in the lab.

Contact Peter Svensson for more information.

We are currently recruiting:

Read more about the positions below:

Financiers

Swedish Research Council

Cancerfonden

Åke Wiberg Foundation

Clas Grochinsky Minnesfond

Läkare mot AIDS Forskningsfond

CIMED

Karolinska Institutet