In response to viral infections, the body uses a wide range of immune mechanisms to protect itself from the invading pathogen. Moreover, in a recent decade it has been appreciated that immune cell signals play a significant part in the regulation of the metabolism and that they are implicated in the development of the various metabolic diseases. In addition, recent studies showed that immune-endocrine interactions have a crucial role in the maintenance of the host physiology and defense. However, the interorgan processes by which immune cells communicate with endocrine cells to coordinate endocrine function and thus to modulate amino acid metabolism during viral infections remains largely unclear. Moreover, what is the purpose of these changes remains fundamentally unexplored. Therefore, our hypothesis is that, in order to minimize the risk of excessive tissue damage and to prevent virus replication, the immune system actively modifies the metabolism of amino acids which boots immune response. Indeed, our research revealed that the immune system during viral infections actively modulates amino acids metabolism, and in particular axis of the homocysteine and cysteine levels. Moreover, we showed that targeting this metabolic pathway helps to modulate the immune response and thus control viral infections. Finally, we confirmed that monitoring and manipulating homocysteine/cysteine levels could be a potential strategy for treatment of viral infections. Therefore, the findings of this thesis will help to clarify the specific mechanisms by which homocysteine and cysteine metabolism regulate immune cell function, cytokine production, and viral replication.