Measles virus infections of the central nervous system

Abstract

Acute measles is a classic infectious disease of childhood with worldwide distribution. Its causative agent, measles virus (MV), is an efficient pathogen, persisting in nature in populations large enough to support it, even though it is able to cause an acute infection in any individual only once in his lifetime. The characteristic clinical hallmarks of measles, fever and rash, coincide with antiviral immune response. MV-specific T lymphocyte and antibody responses contribute to virus clearance and protection from reinfection, respectively. Concomitant with immune activation immunologic abnormalities arise during MV infection. The ensuing suppression of cellular immune responses is presumably responsible for increased susceptibility to other infections. Additionally, central nervous system (CNS) complications of MV infection with different pathogenesis occur. Autoimmune disease may appear in the form of acute measles encephalomyelitis. Furthermore, MV may persist in the CNS in rare cases without periodic shedding of infectious virus. Measles inclusion body encephalitis can develop on the basis of inadequate virus-specific cell-mediated immune responses and subacute sclerosing panencephalitis occurs many years after primary measles as a slow virus infection. Host cell factors operating in cells of the CNS together with mutations particularly in genes coding for viral envelope proteins initiate and maintain the persistent state of infection with a viral replication cycle that is attenuated at the transcriptional and translational level.