Schmallenberg Virus: Pathogenesis, Diagnostic Challenges, and Control Gap in Endemic Europe

Schmallenberg virus (SBV) has evolved from an emergent Orthobunyavirus identified in Europe in 2011 into an endemic pathogen with complex epidemiological dynamics. This review focuses on three key aspects: pathogenesis and fetal neurotropism, diagnostic limitations within the Simbu serogroup, and challenges in disease control. SBV pathogenesis is characterized by immune evasion mediated by the NSs protein and a marked tropism for the developing central nervous system, resulting in congenital malformations when infection occurs during critical gestational stages. Similar mechanisms are shared with other Simbu serogroup viruses, contributing to overlapping clinical presentations and complicating differential diagnosis. Diagnostic approaches are constrained by the short duration of viraemia and significant serological cross-reactivity among related viruses. While RT-qPCR is effective for detecting acute infections, its utility is limited for retrospective diagnosis, where fetal tissues and pre-colostral serology are required. Widely used ELISAs lack serogroup specificity, raising concerns about the potential under-recognition of co-circulating or emerging viruses. Despite advances in vaccine development, implementation remains limited, and vector control strategies provide only partial mitigation. SBV therefore represents a valuable model for understanding arbovirus persistence in temperate regions. Addressing current challenges will require improved diagnostic specificity, sustainable vaccination strategies, and integrated surveillance systems.