Abstract:

Measles virus remains a major cause of childhood mortality, causing a transient immunosuppression that accompanies and follows measles making the patients susceptible to secondary infections accounting for most of measles-related complications and deaths. Majority of measles virus in the body use Signaling Lymphocyte Activation Molecule (SLAM) as a receptor and only a minority of the virus may also use CD46. Infection and subsequent demise of SLAM cells may explain severe immunosuppressive characteristic of this viral disease. Measles also reduces the nonspecific naïve B cells in the bone marrow, which fight unfamiliar infections and SLAM signaling intensifies CD95-mediated apoptosis of B cells.¹⁵ Furthermore, in experimentally infected non-human primates (NHPs) measles virus infects and depletes pre-existing memory lymphocytes, causing immune amnesia. ^{16, 17} Results from different studies offer an explanation for the long-term immunologic sequelae of measles resulting in overall childhood infectious disease mortality.¹⁸ As measles infection is tightly coupled to measles-associated immune memory loss, advancement in research regarding post measles immunological amnesia is needed to investigate regarding immune pathogenesis and host immune responses.

Key Words: Immune amnesia, Signaling Lymphocyte Activation Molecule, Memory B cells and naïve B cells, Memory CD4+ and CD8+ T cells.