Kumao Toyoshima

Enhancement and inhibition of avian sarcoma viruses by polycations and polyanions

Abstract Polycations enhance the infectivity of avian sarcoma viruses for chick embryo fibroblast cultures up to 80-fold. The enhancement is restricted to members of avian tumor virus subgroups B, C, and D and to RSV(O). Subgroup A viruses are either unaffected or inhibited by polycations. The polycation-mediated enhancement is at least in part due to an increased adsorption rate of virus to cell, but may also involve penetration. Viral growth rates are not influenced by cationic polymers. Polyanions reduce the infectivity of avian sarcoma viruses and are also able to neutralize the virus-enhancing activity of polycations. An exception is dextran sulfate which causes virus inhibition only at low concentrations (less than 4 μg/ml), but enhances viral infectivity at higher concentrations. Extracts from normal or leukosis virus-infected chick embryo fibroblasts also enhance focus formation by certain avian sarcoma viruses. The characteristics of this enhancement are similar to that mediated by polycations.

Conditional lethal mutants of avian sarcoma viruses: I. Physiology of ts 75 and ts 149☆

Abstract Ts 75 and ts 149 are two temperature-sensitive mutants of avian sarcoma virus B77 which fail to reproduce and to induce neoplastic transformation at 41°. Both mutants are indistinguishable from wild type in somatic properties of the virion: host range, type-specific antigenicity, and rate of inactivation at 41°. The temperature-sensitive step of ts 75 occurs late in the infectious cycle allowing the synthesis of group-specific antigen in increased amounts and of viral RNA under nonpermissive conditions. Ts 149 has an early temperature sensitive phase and does not produce group-specific antigen at 41°. The maintenance of some neoplastic properties in cells transformed by either ts 75 or ts 149 is continuously dependent on a temperature sensitive viral function: Shift of transformed cells to 41° results in disappearance of neoplastic traits. Double infection of cells at 41° with wild-type avian sarcoma virus and ts 75 or ts 149 results in the rescue of 3 markers derived from the mutant virus: temperature sensitivity, host range, and morphology of the transformed cell. Rescue of ts 75 or ts 149 with wild-type avian leukosis viruses at 41° has not been accomplished.

The reproductive and cell-transforming capacities of avian sarcoma virus B77: Inactivation with UV light

Abstract Avian sarcoma virus strain Bratislava 77 (B77) was irradiated with ultraviolet light, and virus survivors were studied for their ability to transform cells and to reproduce. Two classes of radiation-damaged particles were found. One can still transform but fails to reproduce; the other reproduces but cannot transform. The first class of particles also fails to induce the synthesis of noninfectious virus. It cannot be rescued by superinfection of the transformed cells with an avian leukosis virus, and it is unable to maintain the transformed state during prolonged culture. The second class of particles is antigenically indistinguishable from B77, interferes with avian sarcoma viruses of subgroup C and produces pseudotypes with RSV(0).

Characterization of two strains of avian sarcoma virus isolated from avian lymphatic leukosis virus-induced sarcomas.

Two replication-defective avian sarcoma viruses, S1 and S2, which were independently isolated from tumors of chickens inoculated with avian lymphatic leukosis virus (LLV) were characterized. The genomes of S1 and S2 contain src-related sequences and are, respectively, about 3.9 and 4.5 kilobases long. pp60src-related proteins with molecular weights of 62,000 (p62) were detected in cells infected with these viruses, and protein kinase activity was found to be associated with these proteins. No other viral proteins, such as gag, pol, and env gene products, were detected. These results suggested that the c-src sequence in normal chicken cells was incorporated into LLV genomes by recombination at the expense of most of the viral genes to generate highly defective new sarcoma viruses.