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Co-receptors would subsequently intervene for virus internalization.
For virus internalization, cells were further incubated with virus at 37°C for 30 minutes.
GP is responsible for virus internalization and is then displayed on the external surface of the infected cells.
In addition to these receptors, cell surface molecules, such as epidermal growth factor receptor, ephrin receptor A2 and Niemann-Pick C1-like L1 cholesterol uptake receptor, are also essential for virus internalization.
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Incubation of rIDE with virus prior to infection resulted in increased numbers of VZV genomes inside the cells, compared with virus incubated with a control protein, indicating that rIDE increases virus internalization (P<0.0001 for rIDE vs. P7.5, Fig. 4A).
Although claudin-1 does not appear to modulate the ability of CD81 to bind HCV E2 (data not shown), claudin-1 limits CD81 lateral movement at the plasma membrane and promotes receptor endocytosis (Farquhar et al., 2012; Harris et al., 2012), suggesting a role for the CD81 claudin-1 complex in virus internalization and fusion with early endosomes.
In contrast, there is limited evidence for tight junction protein association with HCV, suggesting an indirect role for claudin-1 and occludin in virus internalization (Meredith et al., 2012).
The sequential engagement of receptors provides a co-ordinated process to regulate virus internalization and offers new targets for anti-viral intervention.
Surface antigen preS of Hepatitis B virus plays fundamental roles in mediating receptor recognition and virus internalization.
It is also unclear whether virus internalization by higher trophic-level organisms has a protective or a detrimental effect on virus viability and transport in pond systems.
To estimate virus internalization, after incubation with labeled virus at 4°C, medium was changed and cells were transferred to 37°C for additional one hour.
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