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Markus Moll group

Photo: Bosse Joha

The battle between the human immune system and many viruses resembles a sophisticated version of hide-and-seek. The immune system is equipped with tools to restrict virus infection, and to sense and eliminate virus-infected cells. Viruses on the other hand have evolved mechanisms to evade restriction, recognition and eradication by the immune system.

The main focus in the group is to investigate functional, molecular and evolutionary aspects of immune evasion strategies evolved by human viruses. The aim of this work is to gain insight into the significance of innate immune mechanisms in successful anti-viral immunity and the relevance of viral immune evasion for establishment of infection and pathogenesis.

Our work is based on a broad spectrum of methods including advanced cell isolation and culture techniques, virus infection under BSL-3 conditions, confocal microscopy and flow cytometry.

Keywords: Viral immune evasion, viral pathogenesis, HIV-1, primate lentiviruses, iNKT cells, CD1d


Markus Moll, Group Leader, Ph.D., Associate Professor

He joined the Center for Infectious Medicine, Karolinska Institutet in 2004. He holds a Ph.D. degree in Virology from the Philipps-Universität Marburg, Germany (2003) and worked as a postdoctoral fellow in Germany, Canada and Sweden. He became an Associate Professor of Experimental Virology at Karolinska Institutet in 2011. In addition to his research commitments, he is course leader for the Introductory Doctoral Supervision Course and the Compulsory Introduction to Doctoral Education at Karolinska Institutet.

Phone: +46-8-585 89686

Lab members

Susanna Bächle, M.Sc., Ph.D. student

She received her Masters degree in Biomedicine from Karolinska Institutet, Sweden, and holds a Bachelor degree in Molecular Medicine from the University of Göttingen, Germany. She got registered as a Ph.D. student in September 2010 and studies molecular and evolutionary aspects of lentiviral interference with innate cellular immunity, in particular invariant natural killer T cells.

Phone: +46-8-585 81158

Past members

Sofia Andersson, Ph.D.

Edwin Heeregrave, Ph.D.

Mirko Kroll, M.Sc.

Sabrina Sibitz, M.Sc.


HIV-1 Vpu interference with cellular receptors

The viral protein U (Vpu) is emerging as an important viral factor for human immunodeficiency virus 1 (HIV-1) to evade restriction, recognition and eradication by the host. Recent findings by us and others have shown that Vpu interferes with the surface expression of host cell receptors to inhibit immune cell activation, migration and homing. We hypothesize that Vpu plays a significant role in HIV-1 evasion from innate and adaptive cell-mediated immunity thereby enhancing viral pathogenicity. The overall goal of our work is to improve our understanding of the interplay between HIV-1 and host immune system with the particular goal to provide a rationale for considering the HIV-1 accessory protein Vpu as a novel target for antiretroviral therapy.

Our studies are summarized in the following projects:

  • Investigating the evolutionary conservation of Vpu-mediated interference with host cell receptor expression and function
  • Identifying molecular and structural determinants of Vpu-mediated modulation of host cell receptors
  • Identifying components of the intracellular trafficking machinery targeted by HIV-1 Vpu to disrupt the surface expression of host cell receptors
  • Exploring ways to inhibit Vpu to boost host cell receptor expression and immune functions in HIV-1 infection

Financial support

  • Swedish Research Council
  • Swedish Physicians Against AIDS Foundation
  • Swedish Medical Society
  • Karolinska Institutet


  • University of Ulm, Germany
  • The George Washington University
  • University of Sao Paolo, Brazil
  • Biotron Limited, Australia

Selected publications









Open positions

We always want to get in touch with talented potential co-workers. If you are interested in doing research within our group, as a degree project or as a researcher, please contact the group leader Markus Moll.