Letter: On competitive innervation of goldfish eye muscles.

be achieved by either homologous mouse type C replicating viruses or heterologous viruses capable of replicating in such cells (8). The increased levels of Moloney sarcoma specific RNA might be achieved by increased rates of transcription of the MSV genome or decreased rates of degradation of the sarcoma specific RNA. In addition, as a secondary effect, increases of sarcoma RNA may occur by gene amplification of the MSV genome. Within an S+Lmink cell infected with helper virus the presence of helper virus reverse transcriptase may increase the copy number of integrated MSV or the pseudotype MSV rescued by helper virus may be superinfecting surrounding S+Lmink cells and thereby increase the copy number. Whatever the molecular explanation, the results observed in cells exogenously infected with Moloney sarcoma virus and superinfected with the replicating type C viruses suggests a hypothesis concerning a similar possible phenomenon in cells that might be carrying latent oncogenic information not acquired by exogenous infection. Thus, it is possible that a usually nontransforming type C virus might act in vivo in a similar manner by leading to an increase in RNA from potentially oncogenic normal cellular or viral genomes during the replication of the nontransforming type C virus. Such a model would predict that some forms of leukemia or lymphoma caused by type C viruses (particularly those characterized by a long latent period and involving replicating but nontransforming viruses) might be due to effects on the levels of RNA of cellular genes by the replicating type C viruses rather than to a direct effect of a transforming gene of the viruses themselves on the growth potential of the cell. PAUL T. PEEBLES EDWARD M. SCOLNICK Laboratory ofTumor Virus Genetics, National Cancer Institute, Bethesda, Maryland 20014 RICHARD S. HOWK Meloy Laboratories, Rockville, Maryland 20850