Round cell variant of measles virus: mechanisms involved in the establishment of defective viral infection of the central nervous system.

During acute CNS infection of newborn hamsters with the LEC strain of subacute sclerosing panencephalitis-derived measles virus, two distinct phases of viral replication occur. The first involves complete replication of the virus with accumulation of cell-free virus, while the second phase is characterized by incomplete viral replication with virus being isolatable only by cocultivation techniques. It has now been shown that the transition between these infection states is associated with a 10,000-fold decrease in the number of infected cells present in the CNS tissue. This finding supports a previously made postulate that the infection state transition results from selective elimination of productively infected cells by host defense mechanisms. Analysis of infected cells from CNS tissues supported this conclusion by demonstrating that cells infected with defective, cell-associated virus could be isolated throughout the infection, even at times prior to the appearance of antiviral serum antibodies. In contrast, cells infected with the most productive form of the virus were found to be largely eliminated very early during the infection, also before the appearance of antiviral antibodies. In vitro experiments suggested that interferon may play an important role in this elimination of productively infected cells and in the establishment of a defective, cell-associated state of infection.