Supplementary Data are available at NAR Online. Asymmetry in the Presence of Migration Stabilizes Multistrain Disease Outbreaks We study the effect of migration between coupled populations, or patches, on the stability properties of multistrain disease dynamics. The epidemic model used in this work displays a Hopf bifurcation to oscillations in a single, well-mixed population. It is shown numerically that migration between two non-identical patches stabilizes the endemic steady state, delaying the onset of large amplitude outbreaks and reducing the total number of infections. This result is motivated by analyzing generic Hopf bifurcations with different frequencies and with diffusive coupling between them. Stabilization of the steady state is again seen, indicating that our observation in the full multistrain model is based on qualitative characteristics of the dynamics rather than on details of the disease model. In this work we study the stability of a multistrain disease model in two coupled populations. Multistrain diseases are diseases with multiple coexisting strains, such as influenza (Andreasen et al. 1997) , HIV (Hu et al. 1996) , and dengue (Ferguson et al. 1999b) . We consider two kinds of strain interactions: cross immunity and antibody-dependent enhancement. When the disease infects an individual, his or her immune system creates serotype-specific antibodies, which will protect the individual against that serotype. 1 However, there is evidence that antibodies also give some cross-protection to the other serotypes (Halstead 2007) . This reduced susceptibility to the other serotypes is temporary. When the temporary cross immunity wanes, heterologous secondary infections are possible. Low level antibodies developed from primary infections are believed to form complexes with the virus so that more cells are infected, and viral load is increased (Vaughn et al. 2000) . This effect is called antibody-dependent enhancement (ADE), and it has been observed in vitro in diseases such as Ebola (Takada et al. 2003 ) and dengue (Halstead and O'Rourke 1977) . Throughout this work we make the hypothesis that ADE increases the infectiousness of secondary infective cases due to the higher viral load Schwartz et al. 2005) . Alternative views of ADE as an increase in mortality associated with secondary infectives can be considered (Kawaguchi et al. 2003) . We focus in this paper on the multistrain disease dengue, which is believed to exhibit both temporary cross immunity and antibody-dependent enhancement (Halstead 2007) .