Abstract
SummaryArbovirus transmission is modulated by host, vector, virus, and environmental factors. Even though viral fitness plays a salient role in host and vector adaptation, the transmission success of individual strains in a heterogeneous population may be stochastic. Our large-scale molecular epidemiological analyses of a dengue virus type 1 population revealed that only a subset of strains (16.7%; n = 6) were able to sustain transmission, despite the population being widely dispersed, dynamic, and heterogeneous. The overall dominance was variable even among the “established” lineages, albeit sharing comparable evolutionary characteristics and replication profiles. These findings indicated that virological parameters alone were unlikely to have a profound effect on the survival of viral lineages, suggesting an important role for non-viral factors in the transmission success of lineages. Our observations, therefore, emphasize the strategic importance of a holistic understanding of vector, human host, and viral factors in the control of vector-borne diseases.
Highlights
Arthropod-borne viruses typically survive through horizontal transmission between vertebrate hosts and biting arthropod vectors such as midges, mosquitoes, and ticks
Considering viral replication in host cells as a surrogate for the fitness, we demonstrate that the variable transmission success of lineages that established sustained transmission is shaped by stochastic forces, which are likely to be influenced by non-viral factors more than the viral fitness and evolutionary differences
The present study reports the analysis of only Dengue virus (DENV)-1, which includes 1,963 E genes and 239 complete polyprotein sequences
Summary
Arthropod-borne viruses (arboviruses) typically survive through horizontal transmission between vertebrate hosts and biting arthropod vectors such as midges, mosquitoes, and ticks. Rapid evolutionary process of DENV is known to select for strains with enhanced adaptation, generating variants that differ in their ability to spread and cause disease (Twiddy et al, 2002b). The differential susceptibility among new viruses against cross-reactive immune responses elicited by preceding serotypes may give rise to serologic-escape mutants that sustain transmission and cause cyclical epidemics (Adams et al, 2006). These observations suggest that the ability of DENV strains to establish transmission in a given locality is influenced by the epidemiological landscape shaped by a combination of viral, immunological, vector, and environmental determinants (Lourenco and Recker, 2010)
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