Most emerging infectious diseases are caused by pathogens that jump from animals to humans, such as Ebola, HIV, influenza and Covid-19. Professor Clare Bryant from the University of Cambridge is using her co-scientist position to look for the molecular switches that cause severe disease in humans, such as sepsis, when pathogens jump between species, and to find novel ways to prevent such phenomena.
Bryant, a testing associate, provided a summary of one of her grant applications to study influenza in birds and humans, outlining her lab’s research questions. The tool generated and classified a set of promising hypotheses—some she had already considered, others she had not. The unknown ones were the most thought-provoking.
When the grant was awarded, Bryant presented a full and detailed proposal. Later, while reading the text on the train to Brussels, she thought “aha!” moment: The co-scientist prioritized a protein that wasn’t on her radar, connected to several signaling pathways she was already interested in. She spent the rest of the week wanting to give him more data.
After returning to the lab, she added unpublished material, kept secret by Co-Scientist. With each iteration, the hypotheses sharpened, moving from candidate proteins to specific amino acids on which her lab could focus its experiments.
Bryant’s team is now building cell lines containing amino acid mutations to test their refined hypotheses. It would typically take two to three years of experimental work to get to the point of identifying the exact amino acids. However, her lab is now on track to complete the project within six months if working with a co-scientist leads them to the right goals.