Abstract
Murine gammaherpesvirus (MHV-68) was isolated from a bank vole. It has
pathobiological and genetic similarities to other gammaherpesviruses including
Herpesvirus saimiri, Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated
herpesvirus (KSHV). It infects laboratory mice and forms plaques on cell
monolayers in tissue culture. The pathogenesis and immunology have been widely
studied in the mouse system and it has been identified as a useful "small animal
model".
Mice were infected with 4xl0⁵ PFU MHV-68 intranasally. The virus infects alveolar
epithelial cells and causes interstitial pneumonia. In the lungs the virus undergoes
lytic replication which is cleared by day 10. Subsequently the virus is found latent in
B cells that have been found to be important in the establishment of latency and in
the transmission of virus from the lungs to the spleen. The spleen and the lymph
nodes at this stage exhibit splenomegaly and lymphadenopathy respectively. In B
cell deficient (μMT) mice, latently infected cells are not detected in the spleen and
splenomegaly is not observed.
In this study, the early events following MHV-68 infection in vivo were examined.
The work focused on the mediastinal lymph node (MEN) that drains the lungs.
Events occurring in the MLNs from the wild type C57BL/6 mice were compared to
those of the pMT mice. The results demonstrated the absence of lymphadenopathy in
pMT 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
pMT 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.
