Hepatitis B virus upregulates host expression of α-1,2-mannosidases via the PPARα pathway

Figure 5 Overall mechanisms of hepatitis B virus escape from host-related immunity with a focus on the role of class I alfa-mannosidases via the PPAR-alfa pathway. Hepatitis B virus infection increases the expression of class I alfa-mannosidases via the PPARα signaling pathway. The surface of HBV envelope proteins could be glycosylated by the class I alfa-mannosidases. In turn, DC-SIGN can no longer recognize the HBV glycoprotein coat, allowing the virus to escape from immune attack. NTCP: Sodium taurocholate cotransporting polypeptide; ER-Golgi: Endoplasmic reticulum and/or Golgi; GlcNAc: N-acetyl-d-glucosamine.