Dynamical Interactions between CTL and Antibody Responses

Part of the Interdisciplinary Applied Mathematics book series (IAM, volume 32)


Chapter 8 discussed how lytic and nonlytic CTL responses influence the outcome of infection, what balance of responses is required to control different infections, and how the occurrence of pathology can be avoided. Much of this discussion focused on one type of immune cell, the CTL, that can perform both lytic and nonlytic antiviral activity. As already mentioned in Chapter 8, however, nonlytic CTL responses effect viral spread in the same way as an antibody response. Like nonlytic CTL responses, antibodies also inhibit the rate of virus spread, without killing the infected cells. Antibodies are a major branch of the immune system, and contribute significantly to nonlytic antiviral activity. However, there is an important difference compared to nonlytic CTL responses. Antibodies are produced by B cells that are a separate population of cells from the CTL. Both B cells and CTL proliferate in response to stimulation by the same virus. Therefore, they are in competition with each other for antigenic stimulation [(2000); (1995a)]. For example, if the CTL response suppresses virus load to levels that are too low to stimulate the B cells, then a successful B cell/antibody response might not be generated. Conversely, if the B cells reduce virus load to levels that are too low to stimulate the CTL, a successful CTL response will not be established. These competition dynamics add complexity to the situation, because the outcome of competition will influence the relative balance between lytic and nonlytic immune responses that fight a given virus.


Virus Load Antibody Response Persistent Infection Antigenic Diversity Virus Population 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Copyright information

© Springer Science+Business Media, LLC 2007

Personalised recommendations