Editorial: Immunometabolic circuits in host-pathogen interaction

The mechanistic interplay between host immunity and pathogen survival is 17 fundamentally governed by cellular bioenergetics (Table 1). Current evidence positions 18 immune cell metabolism not merely as an auxiliary process to generate energy, but as a 19 central regulatory machinery that instructs immune cell fate and effector functions. The 20 Research Topic "Immunometabolic Circuits in Host and Pathogen Interaction" combines 21 seven pivotal studies that elucidate how metabolic networks, micronutrient trafficking, 22 and interkingdom crosstalk operate across different biological scales to determine the 23 clinical outcomes of infectious diseases. 24Viral pathogens exert immense selective pressure on host cellular machinery, frequently 25 inducing profound immunometabolic reprogramming to establish an intracellular niche 26 conducive to replication. The pathophysiological trajectory of severe viral infections is 27 heavily dictated by the host's capacity to maintain bioenergetic homeostasis during 28 systemic inflammation. Recent investigations demonstrate that severe influenza A virus 29 infection triggers massive energy redistributions and oxidative stress, which can be 30 counterbalanced by specific host acute-phase proteins. Experimental models reveal that 31 C-reactive protein executes a critical immunometabolic role during severe H1N1 32 infection by restraining hyperinflammation and preventing fatal metabolic collapse (Luo 33 et al., 2026). This dynamic extends to SARS-CoV-2 pathogenesis, where the clinical 34 severity of COVID-19 is intrinsically linked to the metabolic exhaustion of the innate 35 immune compartment. Patients with severe SARS-CoV-2 infection exhibit a 36 hyperactivated, yet dysfunctional, natural killer cell phenotype, characterized by 37 profound transcriptomic dysregulation (Osuna-Espinoza et al., 2025). Specifically, the 38 pronounced downregulation of key metabolic transcripts, including HIF1A and GLUT1, 39