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Metabolic Reprogramming of Adaptive Immunity Induced by Viral Infections
Guoshuai Tong1,2, Jingwen Dai1, Qianqian Liu1,2
1State Key Laboratory of Animal Disease Control and Prevention, National High-Containment Facilities for Animal Disease Control and Prevention, National African Swine Fever Para-Reference Laboratory, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang Province, China.
None:
Metabolic reprogramming induced by viral infections plays a key role in shaping the efficacy and durability of the host's adaptive immune response. Notably, metabolic reprogramming not only directly governs the differentiation fates of functional subgroups, such as Th1, Th2, Th17, Treg and cytotoxic T cells, but also contributes to supportive immune responses and T-cell exhaustion mediated by metabolic disorders in the context of acute and chronic infections, respectively. Moreover, the metabolic reprogramming of B cells precisely regulates their germinal centre response, plasma cell differentiation and antibody production, thereby modulating the intensity and quality of humoral immunity. Beyond these direct effects, viruses indirectly impair the functionality of T and B cells by altering the metabolic status of innate immune cells such as dendritic cells and macrophages. This review summarises the recent advances of regulatory mechanisms regarding metabolic characteristics of T cells and B cells at various statuses, including rest, activation, differentiation and memory, and discusses immune intervention strategies targeting glycolysis, glutamine and lipid metabolism, and outlines future research directions and clinical translation potential of metabolic reprogramming. A comprehensive understanding of virus-mediated metabolic reprogramming will provide an important theoretical basis for the development of new antiviral therapies and immunotherapy strategies.
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