In this study, the early events following MHV-68 infection in vivo were examined. The work focused on the mediastinal lymph node (MLN) that drains the lungs. Events occurring in the MLNs from the wild type C57BL/6 mice were compared to those of the mMT mice. The results demonstrated the absence of lymphadenopathy in mMT mice and indicated that lymphadenopathy in wild type C57BL/6 mice was brought about especially by the accumulation of B cells. Depletion of CD4+ T cells in wild type C57BL/6 mice demonstrated that the absence of CD4+ T cells only partially affected the accumulation of B cells and enlargement of the MLN. The mMT mouse showed the presence of latent virus in the MLN even in the absence of B cells. However by day 10 these cells were below levels of detection and there was no evidence of systemic transfer of virus. In order to characterise the cells latently infected with virus in the MLNs of mMT mice, a recombinant MHV-68 virus expressing green fluorescent protein (GFP), LHDgfp, was used. LHDgfp has a deletion in the left-hand end and it was therefore characterised in vivo before further studies were initiated. In the MLN and spleen LHDgfp did not show peak latent virus levels as seen with wild type MHV-68, but eventually it was able to establish the same level of latency in these tissues. Therefore LHDgfp was shown to behave similarly to wild type MHV-68 in vivo. The use of LHDgfp helped identify infected cells in the MLNs of mMT mice. Dendritic cells expressing CD11c and macrophages expressing F4/80 were found latently infected in the MLN. LHDgfp was characterised in the IFN a/b receptor knockout system and shown to act like the wild type virus in this immunodeficient host by causing amplification of disease pathogenesis. This system also helped confirm that in the presence of B cells CD11c and F4/80 positive cells were infected very early during infection in the MLN.