Fitting the pieces into a whole picture: physiology and pathogenesis in huanglongbing disease

Huanglongbing (HLB), associated with the phloem-limited bacterium Candidatus Liberibacter asiaticus (CLas), is the most destructive disease affecting citrus production worldwide. Although HLB has been characterized as a phloem-associated disease, causing carbohydrate transport dysfunction, evidence indicates that its effects extend far beyond vascular obstruction and involve complex disruptions in whole-plant physiology. CLas infection affects multiple interconnected physiological processes, beginning with phloem transport, carbohydrate allocation, and source-sink relationships and ending with photosynthesis, water relations, and hormonal regulation, which collectively result in canopy decline, root loss, reduced fruit quality, impaired productivity, and eventual tree death. Recent studies propose that HLB functions as a pathogen-triggered chronic immune disease, in which prolonged host defense responses are the primary mechanism of disease. While this framework provides important insight into the role of reactive oxygen species (ROS) accumulation, callose deposition, and defense-associated signaling in HLB pathology, growing evidence indicates that HLB disease progression involves multiple interacting physiological and pathological processes beyond immune dysregulation alone. This review synthesizes current knowledge regarding the physiological effects of HLB on citrus function, as well as the influence of environmental conditions on disease severity and tree performance. In addition, traits associated with HLB tolerance, including balanced regulation of defense responses, maintenance of phloem functionality, sustained carbohydrate transport, and preservation of hydraulic function under chronic infection pressure, are discussed. Collectively, the evidence supports an integrated view of HLB as a complex systemic vascular and physiological disease resulting from dynamic interactions among bacterial colonization, host defense responses, and disruption of whole-plant physiological homeostasis.