Abstract The North American bison is a keystone species of immense ecological, cultural, and economic importance, yet its long-term stability is increasingly threatened by infectious diseases such as mycoplasmosis caused by Mycoplasma bovis . First recognized in bison in the late 1990s, this disease differs substantially from its presentation in cattle, where M. bovis typically acts as a secondary opportunist. In bison, however, it has emerged as a primary pathogen, causing severe morbidity and mortality within herds, imposing significant economic losses on producers, and jeopardizing conservation and restoration efforts. Despite its profound impact on herd health and sustainability, progress in understanding M. bovis infection in bison has been steady but limited. Major gaps persist in epidemiology, pathogenesis, diagnostic capacity, and effective control strategies. This review synthesizes the current state of knowledge on bison mycoplasmosis, drawing from peer-reviewed literature, government reports, and field management experiences. It addresses epidemiology, clinical and pathological features, diagnostic approaches, and current management strategies. Finally, it highlights key knowledge gaps and outlines future research priorities. The overarching goal is to provide a comprehensive, evidence-based resource for researchers, veterinarians, wildlife managers, producers, and policymakers, while underscoring the urgent need for targeted research to mitigate the threat of M. bovis to North American bison.
Abstract Peste des petits ruminants (PPR) is a major constraint to sustainable small-ruminant production across Africa and Asia, threatening the food security and livelihoods of over 1.5 billion animals. Because of its severe socio-economic impact, the Food and Agriculture Organization and the World Organisation for Animal Health launched the Global Control and Eradication of PPR programme in 2015, aiming for global eradication by 2030. To support this goal, research has focused on transmission dynamics, molecular epidemiology, and particularly the development of improved vaccines and diagnostics. Although current homologous live-attenuated vaccines such as Nigeria 75/1 and Sungri-96 confer durable immunity, they cannot Differentiating Infected from Vaccinated Animals (DIVA), limiting their use in eradication campaigns. This has stimulated the development of next-generation peste des petits ruminants virus (PPRV) vaccines using molecular approaches, including reverse-genetics-based marker vaccines, recombinant viral-vector systems, virus-like particles, and plasmid DNA platforms. This review summarizes recent advances in PPRV vaccine design, emphasizing immunogenic performance, safety, and DIVA compatibility. Integrating structural vaccinology, thermostabilization, and computational antigen design may accelerate the development of field-ready formulations, advancing progress towards the global eradication of PPR – the next disease targeted after rinderpest.
Abstract The adaptive evolution of influenza A virus is strongly influenced by the functional balance between its two major surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA). Although previous studies have demonstrated the importance of HA/NA interplay in receptor binding, virion release, cross-host transmission, and antiviral resistance, most have focused on individual proteins, specific residues, or discrete stages of infection. Consequently, how HA/NA functional balance responds to selective pressures and contributes to viral adaptive evolution remains incompletely understood. Here, we propose a dynamic ‘balance–imbalance–rebalance’ framework centred on the coordination between HA-mediated receptor binding and NA-mediated receptor cleavage. We systematically examine how HA/NA functional balance influences viral attachment, release, and transmission, cross-species adaptation, pathogenicity, immune escape, and antiviral resistance. We further discuss how changes in receptor availability, immune pressure, and antiviral selection may disrupt a pre-existing HA/NA balance and how coordinated changes in HA and NA may compensate for these perturbations to establish new adaptive states. Future studies integrating structural biology, virology, animal models, and large-scale evolutionary analyses will be essential for quantitatively defining the molecular principles and adaptive boundaries of HA/NA coevolution, thereby improving our ability to assess the evolutionary potential and cross-host transmission risk of emerging influenza viruses.
