Various growth phases of Moloney murine sarcoma virus (M-MSV) induced tumors in suckling and young adult BALB/c mice have been studied by light and electron microscopy. In the early phase (3-6 days following M-MSV), observations at the injection site of the thigh muscles consisted of endo- and perimysial edema, «activated» muscle satellite cells, endothelial cells and fibroblasts, scattered type C virus particles within the muscle fibers, muscle fibers and endomysial cells undergoing necrosis and macrophage and granulocyte infiltration. During the overt tumor phase (6-12 days following M-MSV), observation of neoplastic tissue disclosed proliferation of several cell types (endothelial, periosteal, fibroblasts, etc.), poorly differentiated myoblasts along with atypical rhabdo-myoblast-like cells and sarcolytes, type C virus budding from muscle fiber and myoblast plasma membrane, and intense degenerative and regenerative changes in the muscle fibers together with more profuse granulocyte infiltration. The regressive phase (13-21 days following M-MSV) presented reduced cellularity of the neoplastic tissue, a decrease in blast cells, diminishing granulocyte infiltration with contemporaneous appearance of prominent lymphocyte foci and gradual disappearance of virus particles. Although many cell types of mesenchymal origin proliferate following M-MSV infection, the above morphological findings indicate that striated muscle is a preferential site for virus replication and transformation. Furthermore, the peculiar virus cell relationships leading to cell lysis and continuous recruitment of newly infected cells have been widely documented. In the light of these findings it is suggested that, besides the host immune control of virus spread and tumor cell multiplication, the non clonal growth pattern of M-MSV induced tumors is a crucial factor in determining the spontaneous regression which occurs with high frequency in this experimental system.
Genesis of Kirsten murine sarcoma virus: sequence analysis reveals recombination points and potential leukaemogenic determinant on parental leukaemia virus genome
