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Influenza infection and replication is a multi-step process: First, the virus has to bind to and enter the cell, then deliver its genome to a site where it can produce new copies of viral proteins and RNA, assemble these components into new viral particles, and, last, exit the host cell.
These VLPs enter the larval hemolymph along with the egg and rapidly bind to and enter host lamellocytes, ultimately causing them to lyse [27].
The holotoxin can then bind to and enter cells via receptor-mediated endocytosis.
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It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body.
To initiate infection, DENV binds to and enters host cells via receptor-mediated endocytosis [ 40].
However, the mechanism by which aggregated extracellular tau binds to and enters cells to trigger intracellular tau accumulation is still unknown.
The synthetic opioid U-50,488 and the endogenous κ-opioid receptor agonist dynorphin, which is released into the human small intestine during inflammation and appears to bind and enter bacterial cells, have been tested in P. aeruginosa PAO1 and were found to enhance virulence factor production (Zaborina et al., 2007).
Due to the wash step after time periods, it is seen that only few cells manage to bind and enter the cell line between 2 and 3 h.
Particles, unlike single proteins, have the ability to bind and enter cells using appropriate surface receptors.
Adenovirus fiber from most serotypes co-opts the Coxsackie-Adenovirus Receptor (CAR) to bind and enter cells.
The so-called major group of HRV uses intercellular adhesion molecule-1 (ICAM-1) as their receptor [ 173] and the minor group attach to low density lipoprotein (LDL) receptor and very-LDL (VLDL) receptors on epithelial cells in the adenoid area to bind and enter cells [ 174, 175].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com