William T. Lane

Complement-Fixing Antigens in Hamster Tumors Induced by the Bryan Strain of Rous Sarcoma Virus

Hamster tumors transplanted subcutaneously from primary intracranial tumors which developed after inoculation of the Bryan strain of Rous sarcoma virus, contained virusspecific tumor antigens indistinguishable from those induced by the Schmidt-Ruppin strain.

Spontaneous Transformation of Rat Cells After Long-term in Vitro Cultivation and the “switch-on” of a New Complement-fixing Antigen

Summary Rat embryo (RE) cells maintained in tissue culture for long periods developed into tumorigenic lines that exhibited morphological alteration. When tested with broadly reactive anti-MSV rat serum, the spontaneously transformed RE (TRE) cells and tumor cells induced by the TRE cells were positive, however, these cells did not react with guinea pig antiserum which is reactive only with the gs-1 antigen of C-type RNA viruses. While the antigen derived from the TRE line appeared similar to that derived from polyoma transformed RE cell line, it was detected much earlier in the latter cell line. Some characteristics of the new rat cell antigens were described.

Neoplastic Transformation and Derivation of a Focus-Forming Sarcoma Virus in Cultures of Rat Embryo Cells Infected with a Murine Osteosarcoma (FBJ) Virus

Summary Neoplastic transformation of rat embryo cells in vitro by an osteosarcoma (FBJ) virus is reported. Foci of transformed cells consisted largely of spindle-shaped cells which stained vividly with acridine orange. The transformed cells produced virus and complement-fixing (CF) antigen characteristic of the murine leukemia-sarcoma virus complex. Tumors were produced when transformed cells were injected into newborn mice and rats. The mouse tumors had the histologic pattern of osteosarcoma, which was transmissible in cell-free passages in newborn mice. Cell-free extracts of the mouse tumors also produced transformed foci in vitro. The rat rumors were undifferentiated sarcomas, also yielding virus and CF antigens.

Amantadine Hydrochloride: Inhibitory Effect on Murine Sarcoma Virus Infection in Cell Cultures

Summary Amantadine hydrochloride (1 adamantanamine hydrochloride), a compound reported to be active against influenza viruses and Rous sarcoma viruses, inhibited the in vitro cellular transformation induced by Murine sarcoma viruses. The antiviral activity is not due to direct inactivation of the virus.

Neoplastic Transformation of Rat Embryo Cells Induced in Vitro by Rauscher Leukemia Virus

Summary Neoplastic transformation of rat embryo cells in vitro by Rauscher leukemia virus (RLV) is reported. Rat embryo cells infected initially with RLV have replicated infectious virus and produced complement-fixing (CF) antigen characteristic of the murine leukemia-sarcoma virus complex for more than 18 months. Cells from these cultures underwent neoplastic transformation in vitro and produced tumors when injected into homologous hosts. The tumors were serially transplantable, and subsequent transplants continued to carry the initial RLV and to yield CF antigen. The authors wish to thank Mr. H. C. Turner, National Institutes of Health, for supervising CF tests, and Mrs. Ersell S. Richardson and Mrs. M. H. Joglekar for excellent technical assistance. We are also grateful to Dr. L. Rabstein, Microbiological Associates, Inc., for histological examination of tumors.

Occurrence of SV40 neoplastic and antigenic information in vaccine strains of adenovirus type 3.

Summary Adenovirus type 3 strain JF was propagated in its early passage history in rhesus monkey kidney cell cultures. Upon discovery of infectious SV40 in the adenovirus, further passages were carried out in African green monkey kidney cell cultures in the presence of SV40 antiserum. Following this procedure, two separate passage lines of the adenovirus were free of detectable infectious SV40, but vaccine seeds prepared from these lines (JF-1 and JF-2) induced in hamsters tumors which contained CF antigens identical to those found in tumors induced by SV40. These tumors, in turn, elicited serum antibodies that fixed complement with SV40 tumor and T antigens. In addition, both lots of adenovirus 3 strain JF induced the formation in human embryo kidney cells of SV40 antigen which was detected by the immuno-fluorescent technique. The induction of fluo-rescent-stainable SV40 T antigen in tissue culture was prevented by treatment of the virus with adenovirus type 3 neutralizing antiserum but not by treatment with SV40 neutralizing antiserum. This SV40 genetic material was presumably enclosed within adenovirus capsids. The findings are discussed as they related to the use of adenovirus vaccines in man. The authors are indebted to Mr. Horace C. Turner for the performance of the complement fixation tests and to Mrs. Lena Wetherell for technical assistance.