The significance of extracellular enveloped vaccinia (EEV) for the and dissemination of vaccinia virus was investigated. The quantity of released extracellular virus correlated very closely with the ability of 13 vaccinia strains to cause long-range spread of infection (comet formation) in cell cultures infected at low m.o.i. but was not correlated with plaque size. The kinetics of virus spread after low m.o.i. was related to the amount of virus released from primary infected cells but not to their content of intracellular naked vaccinia (INV). Most extracellular vaccinia virus from IHD-J-infected RK-13 cells banded in CsCl density gradients as EEV (88%) while very little banded as INV (2%). Antisera to the envelope prevented comet formation while antisera to INV did not.

CsCl centrifugation of blood-borne extracellular virus from rabbits infected intravenously with vaccinia virus after cyclophosphamide treatment revealed that 64% of the virus banded as EEV but only 11% as INV. High EEV-yielding vaccinia strains were able to spread from the respiratory tract to the brains of mice and cause death. Low EEV-yielding vaccinia strains were generally not able to disseminate or cause mouse mortality. The notable exception to this trend was strain WR, which, although releasing small amounts of virus , could nevertheless very effectively disseminate , causing a high rate of mouse mortality. Treatment with anti-envelope serum protected mice from a lethal vaccinia infection whereas antiserum to inactivated INV did not. These results indicate that the dissemination of vaccinia infection is mediated by EEV and implicate EEV as having a role in the dissemination.


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