Abstract
had no effect of infectivity of HBV. Macropinocytosis could be ruled out as entry pathway of HBV since uptake of the pinocytic marker substrate horseradish-peroxidase (HRP) was efficiently blocked with Ethylisopropylamiloride (EIPA), but had no impact on HBV infection. Agents that prevent endosomal acidification, e.g. Bafilomycin and NH4Cl, were not able to inhibit HBV infection, but blocked infection with SFV very efficiently. Conclusions: These results suggest that in contrast to other viruses, HBV does not use classical clathrinor caveolin-dependent endocytic mechanism for infection, but an unusual endosomal entry pathway that needs to be determined. A low pH within endosomal compartments, important for infection of many other enveloped viruses is not necessary to establish an HBV infection in primary hepatocytes.
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