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Abstract
Simple SummaryThe current coronavirus disease 2019 pandemic turned the attention of researchers to developing novel strategies to counteract virus infections. Despite several antiviral drugs being commercially available, there is an urgent need to identify novel molecules efficacious against viral infections that act through different mechanisms of action. In this context, our attention is focused on novel compounds acting on nuclear receptors, whose activity could be beneficial in viral infections, including coronavirus, hepatitis C virus, and cytomegalovirus.The manipulation of host metabolisms by viral infections has been demonstrated by several studies, with a marked influence on the synthesis and utilization of glucose, nucleotides, fatty acids, and amino acids. The ability of virus to perturb the metabolic status of the infected organism is directly linked to the outcome of the viral infection. A great deal of research in recent years has been focusing on these metabolic aspects, pointing at modifications induced by virus, and suggesting novel strategies to counteract the perturbed host metabolism. In this review, our attention is turned on PPARs, nuclear receptors controlling multiple metabolic actions, and on the effects played by PPAR ligands during viral infections. The role of PPAR agonists and antagonists during SARS-CoV-2, HCV, and HCMV infections will be analyzed.
Highlights
Targeting Metabolism during Viral InfectionsThe viral reproduction needs the host cell machinery for the synthesis of viral components, such as nucleic acids and proteins
Human cytomegalovirus (HCMV) replication is strongly related to host metabolism; the CMV infection alters the activity in multiple metabolic pathways, including fatty acid elongation and lipid synthesis
From HCMV, herpes simplex virus (HSV)-1 shows less reliance on FAS, while its envelope is mainly formed from preexisting cellular material, whereas it upregulates flux from glucose to de novo pyrimidine nucleotide biosynthesis
Summary
The viral reproduction needs the host cell machinery for the synthesis of viral components, such as nucleic acids and proteins. A strict relationship between lipids and HCV is necessary for the mechanism of viral entry into hepatocytes, replication, particles assembly and secretion [46] While lipids and their receptors are key players in the early stages of HCV infection, molecules targeting lipids or their receptors could be considered as novel strategies against HCV infection, by preventing or limiting virus-induced damages [47]. HCMV replication is strongly related to host metabolism; the CMV infection alters the activity in multiple metabolic pathways, including fatty acid elongation and lipid synthesis. From HCMV, HSV-1 shows less reliance on FAS, while its envelope is mainly formed from preexisting cellular material, whereas it upregulates flux from glucose to de novo pyrimidine nucleotide biosynthesis These divergent metabolic strategies represent an important point to interfere with metabolic changes induced by viruses, allowing us to point out different metabolic processes to obtain novel antiviral strategies. Through a combined metabolomic and lipidomic approach, this study demonstrated the impact of the viral UL37x1 protein in remodeling host lipid metabolism
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