ly – the role factors such as temporary cross-immunity and variation in serotype virulence play in epidemics. They found that cross-immunity alone is enough to create the patterns that are observed in nature.
The study is a major departure from other theories about what drives dengue epidemics. The conventional wisdom is that an amplification of the severity of disease caused by repeat infections with different strains, a phenomenon known as antibody-dependent enhancement, drives the boom and bust cycles of dengue epidemics.
"Temporary cross-immunity has been ignored by the epidemiological community," said study co-author Pejman Rohani, associate professor of ecology and UGA Biomedical and Health Sciences Institute researcher.
"It's discussed in the scientific literature," Wearing added, "but no one ever considers it an important factor in generating the epidemiological cycles."
Cross-immunity, which lasts from two to nine months, results when overall antibody levels created by the body in response to infection by one serotype are high enough to protect against infection by related serotypes. After this period, however, antibody levels drop to levels that are no longer neutralizing but instead are exploited by the dengue virus to enhance replication and cause more severe illness.
"You can't deny the empirical fact that people who get severe dengue may well have had cases before," Rohani said. "But our work suggests it's not the mechanism that's underlying the big-picture pattern that we see."
Several factors are contributing to an increase in dengue epidemics. Global warming is allowing the species primarily responsible for spreading dengue (Aedes aegypti, also known as the yellow fever mosquito) to expand its range. Population growth in developing nations is pushing more people into substandard housing in mosquito-infested areas. And the ease of travel brings the virus to areas that were previously
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