Numerous viruses' infection and replication processes are influenced by PTEN-related lipid metabolism. Hepatitis C virus (HCV) impairs the host's lipid metabolism and frequently results in liver steatosis . PTEN protein phosphatase activity affects hepatitis C virus secretion via regulating cholesterol metabolism, and the formation of large lipid droplets enhances viral particle outflow . A translational variation of PTEN is PTEN with a long N-terminal extension (PTEN-L). PTEN-L increases type I interferon response and innate antiviral immunity during viral infection in a phosphatase activity-dependent way . Through the PTEN and AMP-activated protein kinase (AMPK) and dsRNA-dependent protein kinase (PKR)/eIF2 signaling pathways, the p17 non-structural protein of sick avian reovirus induces autophagy to promote virus replication . PTEN activity as a lipid phosphatase promotes dengue fever virus (DENV) generation by the Akt/FoxO1/Maf1 signaling pathway . DENV hijacks the host's lipid metabolism for virus replication, with lipid droplets (LD) playing a critical part in the virus's life cycle . The cholesterol content of the target membrane has a significant effect on the efficacy of membrane fusion mediated by Hantavirus Gn/Gc . Although Hantavirus infection is primarily directed at capillary endothelial cells, virus replication does not appear to cause direct harm to these cells or blood vessels endothelial cells . As a result, vascular damage is likely to occur at the site of Hantavirus infection.