[Truncated] The aim of this thesis was to characterise and examine various mechanisms involved in the development of murine cytomegalovirus (MCMV)-induced myocarditis with a view to develop potential therapeutic regimes. MCMV induces acute and chronic myocarditis in BALB/c mice, which are genetically susceptible to MCMV, and low levels of acute disease in resistant C57BL/6 mice. The role of virus was studied using the laboratory strain of MCMV, K181, and a wild isolate of MCMV, G4. Whilst MCMV is capable of directly killing myocytes, infectious virus is not detectable in the heart beyond day 6 post-infection (p.i.). Myocytes undergo low levels of apoptosis following virus infection, indicating that apoptosis is not a major cause of the necrosis observed in this disease. The inflammatory infiltrate was identified as being predominantly CD8+ T cells in the foci during the acute and chronic phases of disease in both susceptible and resistant mouse strains. CD4+ T cells and B cells were identified throughout the myocardium in both mouse strains, however, only susceptible BALB/c mice mount a macrophage and neutrophil response in the heart following infection.
|Qualification||Doctor of Philosophy|
|Publication status||Unpublished - 2002|