Pathogenesis and virulence of flaviviruses are influenced in vivo by several virus- and host-dependent factors, including the role of defective interfering particles, viral receptors, neurovirulence, immune-response (e.g., antibody-dependent enhancement), and host resistance genes (8).
Cell monolayers were infected with a multiplicity of infection of 0.1 virus per cell to avoid the possible appearance of defective interfering particles characteristic of the high-multiplicity infections with VSV.