Fig. 1.

a) Rhinovirus, as an RNA virus (RV), post-transcriptionally modulates the host cell metabolism. Infection with this virus induces anabolic reprogramming of the host cell metabolism by 1) Inducing PI3K-mediated trafficking of GLUT1-containing vesicles to the host cell membrane thereby increasing glucose uptake. Also, overexpression of GLUT1 has been found to result in increased PPP intermediates 2) Upregulating both glycolysis and glycogenolysis which provides TCA cycle intermediates required for anabolic lipogenesis 3) Activating the PPP which results in enhanced levels of nucleotide that support viral replication. RV: rhinovirus; PI3K: phosphatidylinositol 3-kinase; GLUT: glucose transporter; TCA: tricarboxylic acid cycle. b) Schematic overview representing metabolic targets of some DNA viruses. Various DNA viruses activate particular anabolic metabolic programs following infecting the host cells, to finally support viral replication and virion maturation. Dashed arrows show a virus induced activation of the respective metabolic pathway or a transcription factor activation. TCA: tricarboxylic acid cycle; α-KG: α-ketoglutarate; SREBP: sterol regulatory element-binding protein; ChREBP: carbohydrate-response element-binding protein; GLUT: glucose transporter; HCMV: human cytomegalovirus; HSV-1: herpes simplex virus-1; KSHV: Kaposi's sarcoma-associated herpesvirus; VACV: vaccinia virus.