Figure 1.

Schematic summary of host lipid synthesis and transport pathways used by viruses and bacteria. Compounds that interfere with these pathways and have antiviral or antibiotic activity are indicated. (1) Disruption of lipid rafts affects West Nile virus, Newcastle disease virus, human immunodeficiency virus‐1, and influenza A, bovine parainfluenza, and syncytial viruses and Salmonella typhimurium, Shigella, Mycobacterium avium, Pseudomonas aeruginosa, and Chlamydia trachomatis infection. (2) Inhibition of phospholipase PLA2G4A impairs hepatitis C virus (HCV) replication. (3) Inhibition of 3‐hydroxy‐3‐methyl‐glutaryl‐coenzyme A (HMG‐CoA) reductase by statins interferes with infection of many viruses and bacteria such as West Nile virus (WNV), dengue virus (DENV), tomato bushy stunt virus, Chlamydia pneumoniae, Staphylococcus aureus, Staphylococcus pneumoniae, Mycobacterium tuberculosis, Klebsiella pneumoniae, Escherichia coli, and Coxiella burnetii. (4) Inhibition of acyl‐CoA:cholesterol (Ch) acyltransferase (ACAT) blocks infection of HCV and C. trachomatis. (5 and 6) Inhibition of two different steps of triglyceride (TG) synthesis impairs HCV assembly. (7) When fatty acid (FA) synthase (FASN) is inhibited by C75 or cerulenin, replication of WNV, Usutu virus, DENV, and Flock House virus is blocked. (8) Inhibition of FA‐desaturase stearoyl‐CoA desaturase 1 (SCD1) decreases HCV and DENV infectivity. (9) Blockage of ceramide (Cer) synthesis at two different steps impairs replication of viruses such as WNV, HCV, and hepatitis B virus. (10) Inhibition of the lipid transfer protein Cer transfer protein (CERT) impairs HCV particle release and C. trachomatis infection. (11) Inhibition of sphingomyelin (SM) synthase alters HCV viral cycle. (12) Inhibition of sphingomyelinase (Asm) acts as an antibiotic against S. aureus, P. aeruginosa, Neisseria gonorrhoeae, M. tuberculosis, Mycobacterium smegmatis, E. coli, and C. burnetii. (13) HCV replication decreases when treating with uridine diphosphate–glucose Cer synthase (UGCG) synthetic inhibitors. (14) Inhibition of oxysterol‐binding protein (OSBP) impairs replication of enterovirus, encephalomyocarditis virus, and HCV. (15) Inhibition of Niemann–Pick type C1 protein (NPC1) impedes the entry of Ebola virus and other filoviruses because NPC1 is the specific cell receptor for these viruses; inhibition of NPC1‐mediated Ch transport impairs the replication of DENV, HEV, and HCV viruses and reduces the infection of C. trachomatis, Anaplasma phagocytophilum, and C. burnetii. (16) Inhibition of scramblase phospholipid scramblase‐1 (PLSCR1) reduces herpes simplex virus infection. Biosynthetic processes are compartmentalised in different subcellular locations or organelles. EFE: elder fruit extract; MβCD: methyl‐β‐cyclodextrin; PS: phosphatidylserine; PE: phosphatidylethanolamine; PC: phosphatidylcholine; TCA: tricarboxylic acid cycle; ACC: acetyl‐CoA carboxylase; ChE: cholesterol ester; DGAT1: diacylglycerol acyltransferase 1; DGAT2: diacylglycerol acyltransferase 2; LC‐FACS: long‐chain acyl‐CoA synthetase; MUFAs: monounsaturated fatty acids; PUFAs: polyunsaturated fatty acids; SMS: sphingomyelin synthase; CerS: ceramide synthase; SPT: serine palmitoyltransferase; FAPP2: four‐phosphate adaptor protein 2; GlcCer: glucosylceramide; GSLs: glycosphingolipids; ITZ: itraconazole; PI4P: phosphatidylinositol 4‐phosphate