ORIGINAL

Abstract

Measles is a highly contagious disease caused by measles virus (MV) and continues to be relevant in both public health and cultural conversations. While epidemiological models of MV transmission at the population level are fairly well established and understood, the within-host dynamics of MV infection remain incompletely resolved. In this thesis, we explore these dynamics in more depth by conducting laboratory experiments and modifying existing within-host models to incorporate the dynamics of the chemokine CXCL12 in response to both wild-type and vaccine MV infection. We also conduct a growth curve experiment in order to observe the behavior of wild-type and vaccine strains of MV when grown in vitro. Our results suggest that vaccine viruses proliferate less readily when grown in TLR2 stimulated cells in vitro than wild type virus. We observe higher concentrations of CXCL12 in vaccine-infected cells than in wild-type infected cells. Finally, in the modified model, we see the difference in the dynamics between cells infected with the vaccine and wild-type strains of MV, especially during the immunosuppressed period. The dynamics of CXCL12 mirrors those of susceptible host cells for both wild-type and vaccine models, and these dynamics agree with the experimentally determined data for CXCL12.