Young Scientist of the Month contest 2018 – the first winner!


As you may have heard, QIAGEN is running an ongoing Young Scientist of the Month Contest – it’s an initiative to encourage young scientists with a monthly prize to support their research. The judges select winners based on their research goals and ambitions.

We’re happy to announce that Kwabena Owusu-Boateng is our first Young Scientist of the Month. Kwabena is currently a graduate student at WACCBIP in the University of Ghana. With his prize of $1500 worth of QIAGEN products to advance his study, he will continue his research into host-pathogen co-adaptation, pathogen immune evasion mechanisms and protein–protein interactions that could play a role in the pathogenesis of M. ulcerans. This mycobacterium is responsible for an often-neglected tropical disease called Buruli ulcer.

Buruli ulcer is a chronic, debilitating, necrotizing, infectious disease of the skin and soft tissue. It’s the third most common mycobacterial disease of the immunocompetent host, after tuberculosis and leprosy (1). According to the WHO, the disease is on the increase and has been reported in 33 countries in Africa, the Americas, Asia and the Western Pacific. The mode of transmission to humans remains unknown and there is no prevention for the disease.

Here’s how Kwabena explained the disease and his work: “Lesions are caused by the gradual destruction of the subcutaneous and underlying fat tissues, caused by the bacteria secreting a macrolide toxin. Without treatment, the lesions may ulcerate and spread resulting in severe disfigurement and in extreme cases, auto-amputation of limbs. Despite the increasing global prevalence, the mode of transmission, epidemiology, and mechanism of pathogenesis remain poorly understood. Studies in mouse and mammalian cell lines have shown that like other pathogenic mycobacteria, there exists, within the lifecycle of M. ulcerans, a transient intracellular phase where bacilli infect macrophages and monocytes attracted to the infectious foci. Here, the bacilli are shielded from host immune responses until bacilli become adapted to the host, then the pathogen’s cell lysis machinery is activated resulting in egress of fully replicated bacilli to infect other cells. While trying to establish the role of Acanthamoeba polyphaga in the transmission of the bacteria from the environment to the host, our group observed that while the amoeba cells are able to phagocytize and support replication, the bacilli are unable to lyze out of the amoeba cells – suggesting that transcription of lysis factors in M. ulcerans could be host-specific.”

Making improvements in life possible

QIAGEN is delighted to support Kwabena and the research group at WACCBIP – University of Ghana. Hopefully our support can help to achieve their goal – to elucidate the molecular mechanisms of host susceptibility and intracellular adaptations of the bacteria. According to Kwabena:, “This will be a major step towards identifying new drug and vaccine targets. My project involves the integration of computational and laboratory methods to study host-pathogen co-adaptation and pathogen immune evasion mechanisms, as well as protein–protein interactions, that could play a role in the pathogenesis of M. ulcerans.”

Congratulations to Kwabena and his research group. We wish you well and look forward to seeing you succeed.



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Laura Alina Mohr, M.Sc.

Laura Alina Mohr joined QIAGEN in 2015. She received her Master’s Degree in Chemical Biology at the Technical University Dortmund in Germany. During this time, she was involved in Systemic Cell Biology research at the prestigious Max Planck Institute. Before joining QIAGEN, Laura Alina worked at the Scripps Research Institute, San Diego, where she first focused on DNA damage/repair pathways and telomere biology. Later, she joined the Muscle Development, Aging and Regeneration program at the Sanford Burnham Prebys Medical Discovery Institute. At QIAGEN she is interested in gene expression profiling focusing on various biological pathways, e.g. cancer research and neurodegeneration.

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