Antibody plays a critical role in controlling the spread of coxsackievirus B4 infection, as demonstrated in vitro and in vivo.
The effects of antibody and immune spleen cells of mice on the spread of coxsackievirus B4 in monkey kidney tissue cultures and mice were investigated. The spread of the virus in vitro was decreased both by antibody and by sensitized spleen cells, and the antiviral effect persisted even when the immune serum or immune cells were separated from the virus-infected monolayer by agar. The antiviral effect of the spleen cells was blocked by treatment of cells with antiserum to mouse IgG, but treatment of cells with antiserum to thymocytes had no effect. Non-glass-adherent cells were more capable of limiting the spread of coxsackievirus in cell cultures than were glass-adherent cells. Migration of sensitized splenic leukocytes in vitro was inhibited by specific antigen beginning three or four weeks after various doses of coxsackievirus B4. Adoptive transfer of antiserum protected 80%–100% of recipient mice, but spleen cells from only some of the mice protected 20%–66% of recipient mice against challenge with coxsackievirus B4. Thus, immunized mice develop sensitized T (thymus-derived) and B (bone marrow-derived) cells in the spleen. The B cells elaborate antibody to coxsackievirus, which can act locally to control the spread of infection. These results suggest that antibody plays a critical role in the control of the spread of coxsackievirus infection.
Chaturvedi et al. (1978) studied this question.