Molecular analysis and pathogenesis of the feline aplastic anemia retrovirus, feline leukemia virus C-Sarma.

摘要: We describe the molecular cloning of an anemogenic feline leukemia virus (FeLV), FeLV-C-Sarma, from productively infected human rhabdomyosarcoma cell line RD(FeLV-C-S). Molecularly cloned FeLV-C-S proviral DNA yielded infectious (mcFeLV-C-S) after transfection mammalian cells, and interference studies using transfection-derived demonstrated that our clone encodes FeLV belonging to C subgroup. mcFeLV-C-S did not induce viremia in eight 8-week-old outbred specific-pathogen-free (SPF) cats. It did, however, a rapid, fatal aplastic anemia due profound suppression erythroid stem growth 9 10 inoculated newborn, SPF cats within 3 8 weeks (21 58 days) postinoculation. Thus, genome determinants responsible for genetically dominant induction irreversible aplasia A potential clue pathogenic this comes previous work indicating all isolates subgroup, envelop-gene-determined property, only those are potent, consistent inducers To approach mechanism underlying disease, we first determined nucleotide sequence envelope genes 3' long terminal repeat compared it with FeLV-B-Gardner-Arnstein (mcFeLV-B-GA), subgroup-B consistently induces different myelodysplastic anemia, neonatal Our analysis revealed p15E repeats two strains highly homologous, whereas there major differences gp70 proteins, including five regions significant amino acid apparent substitution. Some these changes also reflected predicted glycosylation sites; protein FeLV-B-GA has 11 sites, which present FeLV-C-S.