Invasion and Evolution of Pathogen Strains Interacting by Partial Cross-immunity.

Ben Adams
(Department of Biology, Faculty of Sciences, Kyushu University)

06/06/13, 13:30 at Room 3631 (6th floor of building 3 of the Faculty of Sciences)


In response to an infection the body produces antibodies specific to the antigenic structure of the pathogen. A template for these antibodies remains after the infection has been cleared. This prevents repeated infection with an identical pathogen. However, these antibodies may not perfectly recognize variant strains with an altered antigenic structure. Then immunity is only partial. Suppose one or more strains, identical except for antigenic structure, are at endemic equilibrium in the host population. How does partial cross-immunity affect the ability of an antigenically variant strain to invade? This is investigated using an epidemiological model. Antigenic space is simplified to one- dimension. Several function forms relating antigenic similarity (or distance) to the strength of partial cross-immunity are considered. If a single strain is at endemic equilibrium any variant that is identical except for its antigenic structure can invade and coexist. When two strains are at endemic equilibrium a third strain may not be able to invade. This depends on the shape of the function relating antigenic distance to partial cross-immunity. If the function has a linear or hyperbolic form invasion is always possible. If it has a parabolic form invasion depends on the antigenic distance between the existing strains, the antigenic location of the invading strain and the basic reproductive number R0. The shape of the immune function determines how the antigenic location of the strains affects the number of secondary infections. The value of R0 determines the importance of tertiary infections. These two components interact to determine when invasion is possible. Some implications of these results are considered including the optimal antigenic location for an invading strain, the optimal antigenic distribution for two strains to resist invasion and the possible antigenic evolution and resultant strain structure.


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