( 2 ) HBV has a circular genome of partially double-stranded DNA within a spherical particle 42 nm in diameter. Hepatitis B virus (HBV) remains an important health challenge in both Western and Eastern cultures with almost 292 million people chronically infected worldwide, ( 1 ) with a substantial percentage of those infected with HBV eventually developing chronic hepatitis, cirrhosis, and hepatocellular carcinoma. endosomal sorting complex required for transport.
Conclusion: These findings implicate the tetraspanin protein CD63 as a marker and an important component in the formation and release of infectious HBV particles. Importantly, the HBV viral particles that were shed from CD63-depleted cells were substantially less infective than those collected from control cells with normal CD63 levels. Consistent with these findings, we found that markedly less LHBs protein was associated with the released HBV particles from CD63 siRNA-treated cells. Small interfering RNA (siRNA)–mediated depletion of CD63 induced a substantial accumulation of intracellular LHBs protein but did not alter the levels of either intracellular or extracellular HBV DNA, nor pregenomic RNA. Immunofluorescence microscopy of HBV-expressing cells showed that CD63 colocalized with HBV proteins (large hepatitis B surface antigens and hepatitis B core) and labeled an exceptionally large number of secreted extracellular vesicles of uniform size. We recently observed that the HBV within infected hepatocytes appears to associate with the tetraspanin protein CD63, known to be a prominent and essential component of ILVs. The intraluminal vesicles (ILVs) generated within MVBs have also been implicated in the late synthesis stages of a variety of pathogenic viruses. It is known that the HBV uses late endosomal and multivesicular body (MVB) compartments for assembly and release. Currently, the hepatocellular trafficking pathways that are used by the hepatitis B virus (HBV) during viral infection and shedding are poorly defined.
0 kommentar(er)
