Rabies is a lethal
viral infection that can
affect almost all
mammals, including
humans. To better understand the replication of
Rabies lyssavirus, we investigated if the
viral load in brains naturally infected with
rabies influences
viral internalization and viral
growth kinetics in
neuroblastoma cells, and if the
viral load affects mortality in
mice after intradermal
infection. We noted that high initial viral loads in brains (group II) were unfavourable for increasing viral titers during
serial passages in
neuroblastoma cells when compared to low initial viral loads in brains (group I). In addition, group I
strains showed higher viral
growth and enhanced internalization
efficiency in
neuroblastoma cells than group II
strains. However, we observed that the dominant
virus subpopulation in group II promoted efficient
viral infection in the
central nervous system in the new host, providing a selective advantage to the
virus. Our data indicate that
rabies infection in
animal models depends on not only the
virus strain but also the amount of
virus. This study may serve as a basis for
understanding the
biologic proprieties of
Rabies lyssavirus strains with
respect to the effects on
viral replication and the impact on
pathogenesis, improving
virus yields for use in
vaccine development.