Role of Macrophages in Wesselsbron and Germiston Virus Infections of Mice

Mice develop age-dependent resistance to intraperitoneal infection with Wesselsbron virus, but not with Germiston virus. This resistance correlates with the capacity of peritoneal macrophages to destroy Wesselsbron virus and is complete by three weeks of age. Macrophages from older mice rapidly inactivated the infectivity of Wesselsbron virus, whereas Germiston virus replicated in these cells. Peritoneal macrophages from older mice protected cell cultures against Wesselsbron virus infection, but macrophages from newborn mice did not. Electron microscopic observations suggested that Wesselsbron virus was actively phagocytosed by macrophages, whereas Germiston virus entered the cells by other means and thus, presumably, circumvented the normal killing mechanisms of these cells. Germiston virus may also have directly impaired these killing functions, however, in that the ability of macrophages to kill phagocytosed Diplococcus pneumoniae was significantly less after macrophages were exposed to the virus.