bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/166082

Selection on non-antigenic gene segments of seasonal influenza A virus and its impact on adaptive evolution

Raghwani, J.·Thompson, R.·Koelle, K.
View original source ↗Export metadata ↓

Abstract

Most studies on seasonal influenza A/H3N2 virus adaptation have focused on the main antigenic gene, haemagglutinin. However, there is increasing evidence that the genome-wide genetic background of novel antigenic variants can influence these variants emergence probabilities and impact their patterns of dominance in the population. This suggests that non-antigenic genes may be important in shaping the viral evolutionary dynamics. To better understand the role of selection on non-antigenic genes in the adaptive evolution of seasonal influenza viruses, we here develop a simple population genetic model that considers a virus with one antigenic and one non-antigenic gene segment. By simulating this model under different regimes of selection and reassortment, we find that the empirical patterns of lineage turnover for the antigenic and non-antigenic gene segments are best captured when there is both limited viral coinfection and selection operating on both gene segments. In contrast, under a scenario of only neutral evolution in the non-antigenic gene segment, we see persistence of multiple lineages for long periods of time in that segment, which is not compatible with the observed molecular evolutionary patterns. Further, we find that reassortment, occurring in coinfected individuals, can increase the speed of viral adaptive evolution by primarily reducing selective interference and genetic linkage effects mediated by the non-antigenic gene segment. Together, these findings suggest that, for influenza, with 6 internal or non-antigenic gene segments, the evolutionary dynamics of novel antigenic variants are likely to be influenced by the genome-wide genetic background as a result of linked selection among both beneficial and deleterious mutations.

Source connections

Explore related subjects

evolutionary biologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Raghwani, J., Thompson, R., Koelle, K.. 2017-07-20. Selection on non-antigenic gene segments of seasonal influenza A virus and its impact on adaptive evolution. https://doi.org/10.1101/166082

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Efficient growth factor production stabilizes cooperation in a cellular public goods game

Eukaryotic cells secrete growth factors that facilitate the proliferation and survival of neighboring cells in a coordinated manner essential for tissue development, repair, and homeostasis. However, mutant cells that fail to produce these factors may exploit the benefits provided by neighboring producers, thereby gaining a proliferative advantage that could lead to the extinction of the producer clone. Evolutionary theory predicts that preventing this "tragedy of the commons" requires a fixed spatial structure or other mechanisms that enable cells to interact preferentially with copies of themselves. Contrary to this expectation, we found that, in competition experiments, cells producing the diffusible growth factor interleukin-3 (IL3) resist invasion by non-producing mutant cells even in well-mixed populations, and that non-producers are driven to extinction instead. Using evolutionary game theory, we show that this outcome arises when the cost-to-benefit ratio of growth factor production falls below a critical threshold. We derive this tipping point analytically across the full parameter space of benefit function shape and group size and confirm that IL3 production in our experimental system satisfies this condition with a production cost less than 0.1% of the benefit conferred. These results demonstrate that efficient public good production alone can resolve the tragedy of the commons in populations of cells, and potentially in other biological systems.

evolutionary biology↗
bioRxiv2026

Repeated Transitions in Migratory Behavior Across a Songbird Radiation Are Not Driven by Selection on Shared Variation in Candidate Genes

Understanding the mechanisms facilitating the repeated evolution of traits is a core question in evolutionary biology. While repeated evolution has been observed across many systems, behavioral phenotypes have been less well studied than morphological traits. Migration is a behavioral adaptation to seasonality that has evolved independently in many animals, and repeated gains and losses of migratory behavior have been especially prevalent throughout the diversification of birds. While migratory traits are heritable in many taxa and candidate genes underlying intraspecific variation in migratory behavior have been identified, whether similar genetic changes are responsible for the repeated evolution of migration remains poorly understood. We used a phylogenomic approach to investigate the relationship between variation in candidate genes and migratory propensity across nearly all species in the parulid warbler radiation (n = 101), a group of songbirds in which migratory behavior has been lost and gained multiple times. Comparisons of candidate gene tree topologies to the parulid warbler species tree revealed cases of discordance, though these were explained by differences in the number of phylogenetically informative sites among genes rather than by elevated genetic similarity among species sharing migratory strategies. Testing models of coding sequence evolution identified sites with elevated dN/dS in five candidate genes, suggestive of positive selection; however, variation at these sites showed no clear association with migratory strategy, nor did we detect recurrent selection across lineages where transitions in migratory behavior most likely occurred. Together, these results contradict the hypothesis that selection on shared variation (ancestral polymorphisms or introgressed alleles) facilitated the repeated evolution of migration in this clade.

evolutionary biology↗
bioRxiv2026

Why development time matters: temperature influences plasticity while nutritional stress reshapes selection and evolutionary potential

The time it takes organisms to reach adulthood is often considered a central life-history trait that influences fitness and is highly plastic across environments. Despite its importance, direct estimates of how selection on development time varies across combinations of environmental stressors remain rare, limiting our understanding of its role in population responses to environmental change. We reared 68 full-sibling families of the vinegar fly, Drosophila melanogaster, at two temperatures (14{degrees}C and 28{degrees}C) on two diets (standard and low-calorie), and measured development time, body size (mass and wing size), egg-to-adult viability and productivity (number of offspring). Temperature caused the largest plastic response, with development taking 4-5 times longer at 14{degrees}C, whereas the low-calorie diet extended development by 20-30%. Yet diet, not temperature, changed directional selection on development time. On the standard diet, faster development was associated with higher fitness at both temperatures. On the low-calorie diet, this advantage disappeared, and at 14{degrees}C slower-developing females tended to produce more offspring. Viability selection showed consistent patterns. The low-calorie diet also increased evolvability in development time c.10-16-fold at both temperatures, and genetic correlations between diets were close to zero, indicating strong genotype-by-environment interactions. Plasticity in development time was not associated with fitness in any treatment. Overall, we provide evidence that development time is a functional trait whose relationship with fitness depends on the environment. Nutritional stress induced a smaller plastic response in development time than temperature, but had a larger effect on directional selection and evolvability. The stressor causing the greatest plastic change in a functional trait is therefore not necessarily the one that shapes its selection and evolution.

evolutionary biology↗