Table 1.

Summary of targets and strategies to control infection and immunity through amino acid metabolism and signalling pathways.

Arg	iNOS-expressing macrophages produce NO from Arg–NO overproduction induces hyperinflammation and local tissue damage: - Arg depletion using arginine-metabolising enzymes limits hyperinflammation and the availability of Arg for viral replication
	Arg1-expressing macrophages provide Pro and polyamines from Arg with immunosuppression that participate to prevent harmful hyperinflammation: - But Arg and polyamines are critical for the virus genome packaging and replication. - Pharmacological antiviral strategy targeting Arg and polyamines should favour the host while restricting Arg and polyamines for virus replication.
Trp	IDO1 causes Trp deprivation in the microenvironment and the generation of immunoactive Kyn metabolites: - Immunosuppressive regulatory effects that inhibits short-term immune response and participate to prevent harmful hyperinflammation.
Gln	Gln is essential for proliferating cells, including lymphocytes, thymocytes, and colonocytes, where it is actively used in several important metabolic processes. - Gln is the precursor for nucleotides and amino sugars. - Gln is degraded by glutaminase to Glu that is further metabolised to g-amino butyrate, glutathione, and folic acid, and is a main source of energy as precursor of intermediates components of the tricarboxylic acid cycle. - The expression of several genes in immune system cells is largely dependent on Gln availability. - Gln depletion alters the balance of the immune response that become more suppressive, by favouring a regulatory T phenotype rather than a Th1 phenotype, associated with an inhibition of IFN‑γ secretion.
Ser	Proliferating activated immune cells are dependent on Ser and activation and differentiation of T cells need enough Ser
Cys	Cys availability is critical for T-cell functions because T cells lack the enzyme converting Met to Cys.
Met	The proper methylation of RNA cap structure of SarCoV2 depends on the level of Met in the host to form SAM: - Restriction of Met availability inhibit viral replication.
Phe	Phe catabolism leads to Phe depletion and the production of H2O2 with antimicrobial toxic effects resulting in the inhibition of microbial growth and to an immunosuppressive activity towards T lymphocytes.
mTOR	Coronaviruses can exploit this cellular machinery for their own protein synthesis and replication: - Inhibition of mTOR can inhibit viral replication.
GCN2	GCN2 senses amino acid starvation and activates downstream pathways that restrict inflammation and viral replication: - Activation of GCN2 can limit hyperinflammation and reduce viral replication.