Hantaan Virus Enters Cells by Clathrin-Dependent Receptor-Mediated Endocytosis

Abstract

The cellular entry of Hantaan virus (HTN) occurs through interactions with beta(3) integrins as cellular receptors. However, the process of HTN infection following attachment to the cell surface is not well understood. Our data indicate that overexpression of a dominant-negative mutant dynamin inhibits HTN internalization and that compounds that block clathrin- but not caveolae-dependent endocytosis also reduce HTN infectivity. In addition, we show that HTN colocalizes with the clathrin heavy chain but not with caveolae. At the early phase of infection HTN colocalizes with EEA-1, an early endosome marker, and later, HTN colocalizes with LAMP-1, a lysosome marker. Cells treated with lysosomotropic agents are largely resistant to infection, suggesting that a low-pH-dependent step is required for HTN infection. These findings demonstrate that HTN enters cells via the clathrin-coated pit pathway and uses low-pH-dependent intracellular compartments for infectious entry.

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“…2A). In addition, treatment of the cells with CPZ to inhibit clathrin-dependent endocytosis (9,27) significantly reduced infection of the cells by RV in a dose dependent manner ( Fig. 2A).…”

A rapid method for infectivity titration of Andes hantavirus using flow cytometry

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“…These results might be explained by the weak interaction between lactoferrin and other cellular molecules rather than heparan sulphate, as the interaction between lactoferrin and heparan sulphate should withstand phosphate buffered saline washing [80]. Further research should be developed to identify whether 3 integrin and/or 1 integrin molecules are binding to lactoferrin [123][124][125].…”