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Emory Researchers Develop Model To Track The Evolution Of Emerging Infectious Diseases

ScienceDaily (Dec. 11, 2003) — With outbreaks of new and frightening infectious diseases such as SARS and monkey pox jumping from the animal kingdom to humans, tracking their spread is vital to public health efforts to contain them. A novel mathematical model developed at Emory University now gives public health leaders another tool to assess the risk of new infectious disease emergence that emphasizes the potentially perilous role of pathogen evolution.

The research led by Emory University biologists Rustom Antia and Roland Regoes, with colleagues from the University of Washington in Seattle and P. & M. Curie University in Paris, appears in the Dec. 11 issue of Nature in their paper "The Role of Evolution in the Emergence of Infectious Disease."

"Tracking the evolution of pathogens is not a new concept, but mutations are usually not taken into account in the models used to assess the emergence of infectious disease. What we have developed is a proposed framework to deal with these mutations that should be kept in mind when developing models for emerging infectious diseases such as monkey pox," says Regoes, lead post-doctoral researcher in Antia's laboratory at Emory.

New pathogens are typically believed to emerge from animal populations when ecological changes increase the pathogens' opportunities to enter the human population and generate subsequent human-to-human transmission.

Current mathematical models used for predicting the spread of emerging infectious diseases in humans operate from the standpoint that diseases stay contained if the basic reproductive number of disease transmissions remains less then one. This means that the average number of secondary infections from persons infected with a disease stays below one. While the disease may still spread to other individuals, the pathogen lines of infection eventually become extinct, preventing the disease from epidemically spreading across the population.

In their Nature paper, the researchers show that factors, such as ecological changes, that increase the basic reproductive number of the potential pathogen (but remaining below one and not at a level sufficient to cause an epidemic) can still greatly increase the length of the random chains of disease transmission. These long transmission chains provide opportunity for the pathogen to adapt to human hosts, and subsequently for the disease to emerge and spread.

"The mathematical model we developed shows that transmission rates of a new pathogen can remain well below an epidemic level, but a disease can still potentially break out dramatically as new strains evolve and become better adapted for human transmission," Regoes says.


Adapted from materials provided by Emory University Health Sciences Center.
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