Multiple Infections and CTL Dynamics

Abstract

When CTL dynamics are analyzed, we usually consider a CTL response in the context of a single specific virus. Upon infection, the CTL response expands, attains effector activity, fights the virus, and differentiates into memory cells. Memory cells survive at elevated levels for a prolonged period of time after the resolution of infection. However, hosts are exposed to a wide variety of infections over their lifespan. Each infection can potentially elicit CTL responses that expand and build memory. This brings up a problem. As the host gets infected by different pathogens, the total number of CTL would increase over time as more and more populations of memory cells are created. However, this does not occur. Instead, experiments have shown that a given infection can result in the decline of the CTL memory population that was established in response to a previous unrelated infection (Fig 6.1) [(2003); (1999; (1996); (1995)]. Thus, already established CTL memory is diminished upon exposure to heterologous antigen. It appears that the second infection activates the CTL memory population that was established in response to a previous infection trough bystander effects. Once activated, however, these CTL do not receive any further survival signals because they are not specific for the antigen that is currently present in the system. Consequently, they die and the population of memory cells declines.