Resistance to and recovery from leishmania infection is dependent on cell-mediated immunity. C57BL/6 mice are resistant to Leishmania amazonensis (La) infection but susceptible to LP-BM5 murine leukemia virus (MuLV) infection. MuLVinfection leads to a state ofimmunodeficiency characterized by severe compromise ofcell-mediated immunity. When infected with La alone, C57BL/6 mice developed a smaU transient lesion that evolved to spontaneous healing or a lesion with extremely slow growth. Lesions were predominantly comprised ofa lympho-macrophagic infiltrate with few parasitized macrophages. When infected with La and, 4 weeks later, with MuLV (La-MuLV), the mice developed a large uncontrolled nonhealing lesion containing vacuolated and heavily parasitized macrophages. In contrast, mice infected with MuLV first and La 4 weeks later (MuLV-La) developed a smaU butpersistent lesion, characterized histologicaly by a smaU number of heavily parasitized macrophages andfew lympbocytes. Eight weeks after MuLV infection, both had similar immunological profiles with decreased lymphocyte proliferation, diminished production ofinterferon-)y, and high production of interleukins 4 and 10. At the time of L. amazonensis infection, La-MuLV animals have a normal T ceU function whereas in MuLV-La mice this function is already impaired,- this may influence the recruitment of macrophages to the site of leishmania injection.