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Fig. 4 | Microbial Cell Factories

Fig. 4

From: Potential use of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition and prevention method in viral infection

Fig. 4

The PCSK9 effect on HCV. Numerous host factors, including heparan sulfate proteoglycans (HSPGs), low-density lipoprotein receptor (LDLR), tetraspanin CD81, claudin-1 (CLDN1), occludin (OCLN), tight junction proteins, receptor tyrosine kinases (RTKs), and the Niemann–Pick C1-like 1 (NPC1L1), are implicated in HCV entry into human hepatocytes. Activation of fatty acid and cholesterol synthesis throughout the HCV life cycle. Throughout its replicative life cycle, HCV fosters a lipid-rich environment by stimulating the expression of transcription factors that are involved in the production of cholesterol and fatty acids. Additionally, HCV increases LDLR expression on the surface of hepatocytes to facilitate entry. Microsomal triglyceride transfer protein (MTP) downregulation further inhibits the excretion of VLDL by HCV [33, 49]

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