The direct effect of the feline leukaemia virus (FeLV) on erythroid colony formation in vitro was investigated. Bone marrow mononuclear cells (BMMC) from FeLV-naïve, specific-pathogen-free (SPF), adult cats were inoculated with FeLVs of characterized strains and biologically cloned subgroups and the subsequent development of colony forming units-erythroid (CFUE) and burst forming units-erythroid (BFUE) and colony forming units-granulocyte-macrophage (CFUGM) was monitored. Exposure to the anaemia-causing Kawakami-Theilen strain of FeLV (FeLV-KT), a phenotypic mixture of subgroups A, B, and C, caused constant depression of day 2 CFUE (to 47% of sham-inoculated controls), day 4 CFUE (41% of controls), and day 10 BFUE (38% of controls). CFUGM were unaffected. The lymphoma-causing Rickard strain of FeLV (FeLV-R-TL) caused sporadic depression of CFUE and BFUE. In contrast, neither FeLV-R passaged through feline embryonic kidney fibroblasts (FeLV-R-CRFK) nor biologically cloned, subgroup-specific, FeLVs of fibroblast origin, caused decrements in CFUE or BFUE, suggesting that fibroblast passage attenuated the direct erythrosuppressive effect of FeLV. Suppression of CFUE and BFUE by lymphoma cell-origin FeLV was dependent on infectious virus and was associated with FeLV replication by the cultured myelomonocytic precursor cells. Attenuation of infectivity by heat or u.v. restored CFUE and BFUE development. Examination of the relationship between viral infectivity (VI), viral protein concentration, and CFUE suppression showed that the infectious FeLV was 20-fold more effective than u.v.-inactivated FeLV as an inhibitor of erythrogenesis in vitro.