DENV-1 NVP-BKM120 lineage replacements were observed in Myanmar, Cambodia, Thailand in the late 1990s, in the mid-1990s and in the early 2000s respectively. Similarly, DENV-2 lineage replacements were observed in Vietnam in the early 2000s. DENV-3 lineage replacements were observed in Sri Lanka in the late 1980s, and in Thailand in the early 1990s. And DENV-4 lineage replacements were observed in Puerto Rico during the 1980s and 1990s. A more global lineage replacement event has also been reported, in which DENV-2 lineages from Southeast Asia displaced the American DENV-2 lineage in the Americas during the early 1990s. Exploring the causes of DENV lineage replacement has important implications for dengue epidemiology and control. As DENV antigenic properties often differ between lineages, understanding the mechanisms that underlie lineage turnover will influence vaccine design, and the putative mechanisms of lineage replacement are used to develop prediction models for future dengue epidemics. Despite this potential significance, there are multiple explanations exists on whether lineage replacement events result from the random sampling of viral variants during genetic bottlenecks due to the stochastic nature of DENV transmission, or from variations in fitness within discrete viral populations. For the purposes of this work, fitness is defined as the ability of DENV-1 virions to replicate in cultured cells. Some phylogenetic studies have suggested that observed DENV lineage replacement events were due to either a higher viraemia in the human host or enhanced infectivity in mosquito vectors, while others suggested that the data were more consistent with stochastic events. With respect to viral fitness in other systems, fewer than 5% of members of Vesicular stomatitis virus populations were reported to be more fit than the population from which they were drawn, and mixtures of Ross river virus populations containing less than 1% of a virulent strain nonetheless displayed a virulent phenotype. Despite these observations, the distribution of fitness in DENV populations has been not yet been quantified and correlated with epidemiological patterns, like lineage extinction and replacement during transmission. Here, we measured distribution of fitness within DENV populations with differing epidemiological histories and correlated them with observed lineage extinction and replacement events. DENV lineage turnover is commonly observed in DENV evolution, but it is unclear whether lineage replacement events are caused by selective pressure or by random sampling during transmission. While DENV populations are highly diverse, the overall fitness of a DENV population in an individual host is unlikely to be simply the sum of individual fitness. Other similarly diverse arboviruses exhibit characteristics consistent with synergy within their viral populations.