ALEUTIAN MINK DISEASE PARVOVIRUS INFECTION OF MINK MACROPHAGES AND HUMAN MACROPHAGE CELL-LINE U937 - DEMONSTRATION OF ANTIBODY-DEPENDENT ENHANCEMENT OF INFECTION

Aleutian mink disease parvovirus (ADV) infects macrophages in adult mi nk. The virulent ADV-Utah I strain, but not the cell culture-adapted A DV-G strain, infects mink peritoneal macrophage cultures and the human macrophage cell line U937 in vitro. However, preincubation of ADV-G w ith ADV-infected mink serum enhanced its infectivity for U937 cells. T he enhancing activity was present in the protein A-binding immunoglobu lin G fraction in the serum, but F(ab')2 fragments failed to enhance t he infection. On the other hand, the same sera inhibited ADV-G infecti on of Crandell feline kidney (CRFK) cells. Although U937 cells were no t fully permissive for antibody-enhanced ADV-G infection, ADV mRNA exp ression, genome amplification, and protein expression were identical t o those found previously for ADV-Utah I infection of U937 cells. Prein cubation of ADV-Utah I with soluble protein A partly inhibited the inf ection of U937 cells but did not affect infection of CRFK cells. In mi nk peritoneal macrophages, preincubation with the infected mink serum did not make ADV-G infectious. However, the infectivity for mink macro phages of antibody-free ADV-Utah I prepared from the lungs of infected newborn mink kits was enhanced by ADV-infected mink serum. Moreover, protein A partly blocked ADV-Utah I infection of mink macrophage cultu res. These results suggested that ADV-Utah I enters mink macrophages a nd U937 cells via an Fc receptor-mediated mechanism. This mechanism, a ntibody-dependent enhancement, may also contribute to ADV infection in vivo. Furthermore, since ADV infection in mink is characterized by ov erproduction of anti-ADV immunoglobulins, antibody-dependent enhanceme nt may play a critical role in the establishment of persistent infecti on with ADV in vivo.