Abstract
MCALLISTER et al.1 recently reported the observation of a type-C virus released from cultured human rhabdomyosarcoma cells following passage in foetal kittens. The parent cell line (RD cells) contained no virus before passage. However, a cell line, RD114, established from a brain tumour in an inoculated kitten released particles with morphological and biological properties of a mammalian RNA tumour virus. The obvious explanation that the appearance of RD114 virus (RDV) represented an infection of the human RD cells by an endogenous feline oncornavirus was undermined by the observation of striking antigenic and biological differences between RDV and known feline viruses. Briefly listed, these differences included the observation that: (1) RDV grows well on human and primate cells but not on feline cells1; (2) the group-specific antigen of known feline type-C viruses was absent from RDV as were feline envelope antigens as judged by interference and viral neutralization tests; further, antigens of other known mammalian type-C viruses were not detected, with the exception of the interspecific antigen (gs-3)1,2; (3) the constituent RNA-dependent DNA polymerase of RDV did not react with antisera against feline leukaemia virus (FLV) DNA polymerase and other mammalian viral DNA polymerases3; (4) the molar base ratio of the high molecular weight RNA genome of RDV differs significantly from that of the FLV released from RD cells infected with FLV4. Thus, the suggestion was made that RDV might be a human type-C virus originating from the rhabdomyosarcoma cells of the RD cell line1.
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