Host age and cell type influence measles virus protein expression in the central nervous system.

Measles virus infection of the central nervous system (CNS) of children can result in a slow, progressive fatal disease, subacute sclerosing panencephalitis (SSPE). The pathogenesis of persistent measles virus infection of the CNS has been studied by comparing viral protein expression in suckling or weanling hamsters infected with the HBS strain of measles virus. Suckling animals develop a rapidly progressive fatal encephalitis while weanling animals survive and are persistently infected. Viral nucleocapsid (NP) and hemagglutinin (H) proteins have been examined during acute infection in suckling and weanling animals. Viral H protein expression is selectively inhibited in infected neurons of weanling animals, while infected ependymal cells retain the capability to express H protein at the cell surface; suckling animals express high levels of both proteins. Anti-measles antibodies are not responsible for the inhibition of H protein since immunosuppression does not restore protein expression. The cell-associated virus which is recovered late in infection by co-cultivation with Vero cells expresses all viral proteins. These results suggest that intact viral genome is present in persistent infections, and cell type or state of differentiation of infected cells may be instrumental in expression of viral proteins which can influence lytic or persistent outcome of infection.