Alterations in cellular polyamine metabolism during viral infections

Viruses exploit the host cell machinery, forcing cells to produce viral proteins and other components required for the formation of new viral particles. Polyamines (PAs) are universal polycations essential for both vital cellular processes and viral replication. However, the optimal intracellular PA levels required for viral activity may vary among viruses, as both increases and decreases in PA levels may differentially affect viral replication and survival. Excessively high PA levels may exert antiviral effects by inhibiting some viral enzymes. Different viruses can employ distinct strategies to maintain the PA levels required for the efficient replication. Virus-infected cells are often characterised by the simultaneous activation of PA biosynthesis and catabolism, a phenomenon that may be regarded to as a metabolic dysregulation. However, a closer examination of the role of PAs at different stages of the life cycle of individual viruses may reveal the biological rationale underlying these changes in PA metabolism. PA biosynthesis in virus-infected cells relies mainly on arginine via classical and alternative pathways. Some evidence suggests that viruses may also utilise proline (Pro) as a precursor for PA biosynthesis. This review focuses on clinically important viruses whose effects on host cell PA metabolism have been studied most extensively. We compare how these viruses alter host cell PA biosynthesis and degradation in relation to the functions of PAs during their life cycle.