Virion expression in filtrates of lymphomas in AKR/J or C3H/HeJ mice was assayed by two techniques: (a) in vitro infectivity (XC assay), or (b) acceleration of oncogenicity in vivo (O assay). The two assays appeared to detect different virus populations or activities. This was shown when the same filtrates were tested in parallel by the XC and O tests and opposite results were obtained on the two assays, e.g., XC + O- or XC- O+.

It was postulated that two viruses, termed “XC+” and “O” to correspond to the assays used to detect them, were involved in oncogenesis. When lymphomas originally virus induced were passaged by cells in 2- to 3-month-old syngeneic AKR or C3H mice, oncogenic activity of filtrates of these transplanted lymphomas decreased as cell passages increased. These filtrates from C3H lymphomas also had decreased XC activity as cell passages increased. Normal lymphoid tissue from 1- to 5-month-old AKR mice was XC+ O-, while from C3H mice it was XC- O-. Thus, the two strains modified activities lacking in their normal tissues.

Filtrates highly oncogenic in XC+ newborn AKR mice were oncogenic in C3H newborn mice only when sufficient XC+ virus was in the inoculum received by the XC- C3H mice. Thus the XC+ virus appeared to play a synergistic role with a postulated O virus in oncogenesis.


Supported by Research Grants CA 13467, CA 13468, and CA 12386 from the National Cancer Institute and by Contract AT (04-1) GEN 12 between the Atomic Energy Commission and the University of California.

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