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Experiments have shown that hepatitis C virus (HCV) infections in vitrodisseminate both distally via the release and diffusion of cell-free virusthrough the medium, and locally via direct, cell-to-cell transmission. Todetermine the relative contribution of each mode of infection to HCVdissemination, we developed an agent-based model (ABM) that explicitlyincorporates both distal and local modes of infection. The ABM tracks theconcentration of extracellular infectious virus in the supernatant and thenumber of intracellular HCV RNA segments within each infected cell over thecourse of simulated in vitro HCV infections. Experimental data for in vitro HCVinfections conducted in the presence and absence of free-virus neutralizingantibodies was used to validate the ABM and constrain the value of itsparameters. We found that direct, cell-to-cell infection accounts for 99%(84%$-$100%, 95% credible interval) of infection events, making it the dominantmode of HCV dissemination in vitro. Yet, when infection via the free-virusroute is blocked, a 57% reduction in the number of infection events at 72 hpiis observed experimentally; a result consistent with that found by our ABM.Taken together, these findings suggest that while HCV spread via cell-freevirus contributes little to the total number of infection events in vitro, itplays a critical role in enhancing cell-to-cell HCV dissemination by providingaccess to distant, uninfected areas, away from the already established largeinfection foci.

Quantifying the relative contribution of free virus and cell-to-cell  transmission routes to the propagation of hepatitis C virus infections in  vitro using an agent-based model