Research interests

Our Autophagy-directed Immunity (ADI) research group focuses on elucidating the mechanisms governing autophagy pathways, ultimately aiming to maximize the therapeutic potential of targeting autophagy to intervene in chronic viral infections and inflammatory diseases. Autophagy pathways are not only endowed with the capacity to degrade viruses and instruct adaptive T cell-mediated responses, but also to mediate the release of cytosolic contents extracellularly and thereby control inflammatory output. We use both hypothesis-driven as well as unbiased genome-wide and proteomics approaches to define novel regulators and signalling components of autophagy pathways. In this context, we have recently discovered an important role for autophagy in restricting HIV-1 infection through a novel TRIM5α-Atg16L1-Atg5 mechanism. Currently, we are investigating the impact of the TRIM5α-mediated autophagy pathway on HIV-1 disease progression and inflammatory signatures.


Our major research lines are:

  1. Molecular Regulation of Degradative Autophagy and Secretory Autophagy in Viral Infections, with particular emphasis on HIV-1 and Dengue virus infection.  
  2. Function of Autophagy Molecules and Autophagy Vesicles on Virus Restriction, Molecular Inflammation and T-cell mediated Immunity - using organoid technology and ex vivo explant tissue models.
  3. Impact of Autophagy Mechanisms and Polymorphisms on Clinical Disease Outcomes


Current members:

  • Renée RCE Schreurs       - Postdoctoral fellow 
  • Alexandra PM Cloherty  - PhD candidate
  • Tracy-Jane THD Eisden  - PhD candidate [Alliance AMC-VUmc joint project]


For any enquiries, please contact:




Immunology, Cellular & Molecular Biology, Virology, Autophagy

Research output

  1. Vaginal bacterium Prevotella timonensis turns protective Langerhans cells into HIV-1 reservoirs for virus dissemination

    Research output: Contribution to journalArticleAcademicpeer-review

  2. Autophagy-enhancing drugs limit mucosal HIV-1 acquisition and suppress viral replication ex vivo

    Research output: Contribution to journalArticleAcademicpeer-review

  3. HIV-1 subverts the complement system in semen to enhance viral transmission

    Research output: Contribution to journalArticleAcademicpeer-review

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