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This review demonstrates how viral infections alter GABA and NMDA receptor functions, indicating potential therapeutic targets for immune and neurological disorders.
Gamma-aminobutyric acid receptors (GABARs) primarily function by suppressing inflammatory responses, modulating neuronal excitability, and maintaining intracellular homeostasis, whereas N-methyl-D-aspartate receptors (NMDARs) play a key role in mediating pathological processes through the regulation of excitatory neurotransmission and immune responses. Viral infections have the capacity to modify the expression and functionality of these receptors, either directly or indirectly, thereby contributing to dysregulation within the neurological and immune systems and triggering a range of disease states. This review offers a comprehensive analysis of the mechanisms through which various viral infections interact with GABARs and NMDARs, emphasizing the possible intricate roles these receptors play in viral pathogenesis. Additionally, it underscores their potential as therapeutic targets for antiviral interventions, particularly in addressing immune dysregulation and neurological disorders.
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Ning et al. (2025) studied this question.
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