Antibody-mediated infection of P388D1 cells with 17D yellow fever virus: effects of chloroquine and cytochalasin

Antibody-mediated 17D yellow fever virus infection of a murine macrophage-like cell line, P388D1, was not inhibited by concentrations of cytochalasin B which did inhibit phagocytosis of antibody-coated sheep red blood cells. Chloroquine did not affect antibody-mediated enhancement of viral growth but inhibited viral replication equally whether infection was carried out in the presence or absence ofantibody. The results uggest that the route of internalization of virus and subsequent intracellular pathways of replication are similar for both conditions of infection. Cytochalasin B inhibits phagocytosis ofbacteria (Malawista et al., 1971; Davies et al., 1973), inert particles (Axline & Reaven, 1974) and antibody-coated sheep red blood cells (Diamond et al., 1978) but does not interfere with the ability of Sindbis or vesicular stomatitis (VSV) viruses to infect or to replicate in BHK-21 cells (Coombs et al., 1981). This observation has been taken as evidence that the route of internalization fthese viruses is not by phagocytosis. Chloroquine inhibits replication of Sindbis, VSV (Coombs et al., 1981) and Semliki Forest viruses (Helenius et al., 1980) in BHK-21 cells. Evidence has been presented hat chloroquine and other lysosomo-tropic weak bases do not affect cell membrane attachment or the rate ofendocytosis ofSemlik