Abstract
Original antigenic sin is the phenomenon in which prior exposure to an antigen leads to a subsequent suboptimal immune response to a related antigen. Immune memory normally allows for an improved and rapid response to antigens previously seen and is the mechanism by which vaccination works. I here develop a dynamical system model of the mechanism of original antigenic sin in influenza, clarifying and explaining the detailed spin-glass treatment of original antigenic sin. The dynamical system describes the viral load, the quantities of healthy and infected epithelial cells, the concentrations of naïve and memory antibodies, and the affinities of naïve and memory antibodies. I give explicit correspondences between the microscopic variables of the spin-glass model and those of the present dynamical system model. The dynamical system model reproduces the phenomenon of original antigenic sin and describes how a competition between different types of B cells compromises the overall effect of immune response. I illustrate the competition between the naïve and the memory antibodies as a function of the antigenic distance between the initial and subsequent antigens. The suboptimal immune response caused by original antigenic sin is observed when the host is exposed to an antigen which has intermediate antigenic distance to a second antigen previously recognized by the host's immune system.
Highlights
An immune memory comes from a previous infection or vaccination, stores the information for antigen recognition, and is activated in a future infection by a related pathogen
The present study aims to use a set of ordinary differential equations (ODEs) to describe the interaction among the B cells, the virus particles, and the epithelial cells
Model Development and Description I use a simplified model consisting of the major components of an immune response, which are epithelial cells, influenza A viruses, and an immune system, to describe the dynamics of an influenza A infection and the subsequent immune response
Summary
An immune memory comes from a previous infection or vaccination, stores the information for antigen recognition, and is activated in a future infection by a related pathogen. By recognizing and rapidly eliminating the reinfecting pathogen, this long-lasting effect can permanently or temporarily prevent the reinfection of the host by some pathogens [6]. In some cases, this long-lasting effect can reduce the severity, duration, or risk of the infection and symptoms [7]. Called variola virus, only propagates in humans and has a relatively low mutation rate [8]. Influenza A virus propagates in humans, pigs, and aquatic birds, with a higher mutation rate that is approximately 2:0|10{6/ nucleotide/infectious cycle [9], or 1:6|10{5/amino acid/day. For influenza A, there is usually a significant antigenic distance between the circulating strain in a given year and the immune memory from previous years
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