Chikungunya virus (CHIKV) is an arthropod-borne alphavirus that causes an abrupt febrile illness typically marked by intense arthralgia, rash, and profound fatigue. Following transmission predominantly through Aedes mosquitoes, the virus is able to infect a broad range of host cell types, such as fibroblasts and macrophages, resulting in acute viremia with high viral titers and, in a subset of patients, prolonged arthritis-like manifestations. CHIKV carries a positive-sense, single-stranded RNA genome that encodes nonstructural proteins essential for viral replication as well as structural components required for virion assembly and host-cell entry. The MXRA8 receptor has recently been identified as a central determinant of viral entry and cellular tropism. Genomic analyses place CHIKV into three major lineages, and certain amino-acid substitutions, most notably the E1-A226V change, have been linked to improved adaptation to Aedes vectors and more efficient transmission. The host immune reaction is multifaceted, involving type I interferons, neutralizing antibodies, and virus-specific T-cell activity. Even so, the virus is able to bypass several of these defenses through established evasion mechanisms, which may contribute to prolonged infection in some cases. Given the continued expansion of Aedes mosquito populations driven by climate change, integrated vector-management strategies remain essential. These include chemical, biological, and genetic approaches aimed at curbing mosquito densities and reducing the impact of insecticide resistance. Sustained global surveillance and coordinated public-health interventions are critical to mitigating the growing burden of CHIKV and addressing the recent surge in large-scale outbreaks.

The Varroa mite (Varroa destructor) has reshaped the viral landscape of honey bee colonies, significantly contributing to colony mortality. In response, Varroa-resistant honey bee breeding programs have developed as a promising and sustainable long-term strategy to control Varroa mite infestations in managed colonies. These breeding programs drive the coevolution of hygienic bees and Varroa mites, however the impact of such coevolution on bee and mite viral dynamics remains poorly understood. To address this gap, we investigated how Varroa-resistant traits influence the tripartite interaction among honey bees, Varroa mites, and viruses. Two apiaries were established: one in Greensboro, North Carolina, consisting of high and low UBeeO colonies, and another in Stoneville, Mississippi, consisting of Pol-line and Commercial colonies. Worker bees and Varroa mites were collected from each colony throughout the beekeeping season and screened for 7 viruses. Hygienic selection significantly reduced the Varroa mite infestation level and influenced the dynamics of viruses in worker bees and Varroa mites. Specifically, titers of Varroa-associated viruses were significantly reduced in worker bees and in mites collected from hygienic colonies. Additionally, hygienic selection altered the co-occurrence patterns and correlations among multiple critically important viruses in mites and worker bees. These findings highlight the value of selective breeding as an effective strategy for improving honey bee health and colony survival and shed light on the complex tripartite relationships between honey bees, Varroa mites, and viruses.