DrCatherine Kibirige

After a recent secondment as a Research Manager, Dr. Catherine is now serving as an Intellectual Property Strategy Officer within the Imperial Enterprise Division. Her duties involve overseeing compliance with UK Government research security regulations, including export control licensing and national security investment notifications; managing the Reward to Inventors Scheme to ensure accurate distribution of commercialisation revenue to researchers; facilitating the transfer of non-commercialised IP to inventors pursuing independent commercialisation; conducting due diligence on student IP disclosures and issuing IP clearance letters.

As a Research Scientist, Catherine has been involved in HIV-1 clinical research alongside large epidemiological cohort studies for over 20 years. Previous research projects involved establishing 'The HIVQuant Project'; updating and field-testing an ambient-temperature HIV-1 quantification kit for early infant-diagnosis, treatment-monitoring and cure-related research. The kit was specifically designed for resource-constrained settings. Dr. Kibirige undertook an extensive market discovery exercise through the UKRI ICURe program as well as engaging in biomedical commercialization accelerator programs.

Dr. Kibirige's research activities in the past have included the molecular characterization of the HIV Infection event and profiling of CD8-mediated killing. Developing ultra-sensitive HIV-1 total nucleic acid and integrated DNA qPCR assays and integration-site profiling protocols.

Dr. Kibirige also worked on a study related to transmitted founder infectious molecular clones with defined replicative capacity, that have been shown to define early HIV-1 pathogenesis. Using a qualitative viral inhibition assay (VIA), a negative correlation was deciphered between viral replicative capacity and CD8 T cell mediated viral inhibition. The research hypothesis was that high HIV replicative capacity is associated with higher HIV RNA kinetics and a transcriptomic profile that indicates greater viral success in hijacking host replicative cellular functions and suppression of host immune recognition.