How human behaviour spreads infectious diseases

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A study from the University of Waterloo shows how mathematics can influnce human behaviours that lead to the spread of infectious disease. Current models used to predict the emergence and evolution of pathogens within host populations do not include social behaviour. People treat disease systems in isolation from social systems and don’t often think about how they connect to each other.

Social reactions to infectious diseases can influence which strains become prominent in the population. Adding dynamic social interactions to the models already used for disease outbreaks and evolution could give better anticipate how a virulent pathogen strain may emerge based on how humans attempt to control the spread of the disease. This new addition to disease modelling could allow scientists to better prevent undesirable outcomes, such as more dangerous mutant strains from evolving and spreading.

The social modelling could impact public health responses to emerging infectious diseases like Ebola and Severe Acute Respiratory Syndrome (SARS). Human behaviour during these outbreaks often changes dramatically during the outbreak. People may start using face masks, or stop using them prematurely. Also, public fear of the pathogens may end up driving the wrong type of behaviour if the public’s information is incorrect. The modelling could help public health responses navigate and better channel these kinds of population responses,

The new mathematical model formulated by researchers to study the influence of social behaviour on the competition between pathogen strains with different virulence. Using computer simulations, they analyzed how the model behaved under various possible scenarios that might occur to populations to explore the logic of the hypothesis that social behaviour plays a role in the evolution of the strain.

According to Pharaon, a PhD candidate at Waterloo’s Faculty of Mathematics, human behaviour plays a big role in the spread and evolution of an infectious disease. The model formulated was a general model, but it could be adapted with more biological detail and structure for more specific pathogens.

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