A kinetic model for virus binding which involves release of cell-bound virus-receptor complexes.
A general kinetic mechanism is presented for reversible binding of viruses to cells followed by an irreversible step that initiates the delivery of the viral genome. A novel feature is additional pathways for the release of both virus-occupied and unoccupied receptors from cells. Due to one simplifying assumption, it does not apply at low receptor densities. However, it is sufficiently general to be applicable to ligand binding and internalization for those systems in which ligand diffusion is rate limiting. Three different versions of the model fit the usual kinetic data for the binding of an eclipse mutant of bacteriophage phi X174 to Escherichia coli. However, in each case binding to cell-bound receptors is irreversible. Therefore, this explains the apparent failure of this system to obey the Law of Mass Action. One version of the model also predicts that the release rate of lipopolysaccharide receptors from the outer membrane may be significantly lowered when virus is bound to these receptors.
D010584:Bacteriophage phi X 174 / Q000502:physiology*; D003201:Computers; D004926:Escherichia coli / Q000378:metabolism*; D007700:Kinetics; D008954:Models, Biological; D011991:Receptors, Virus / Q000378:metabolism*
D011991:Receptors, Virus