Abstract
Mouse spleen cells which normally cannot support the in vivo replication of vesicular stomatitis virus (VSV) became susceptible to VSV infection after the intraperitoneal growth of certain syngeneic and allogeneic tumors. After 3 days' growth of P815 tumor cells in syngeneic DBA/2 mice, the viral-permissive state for VSV replication had been established. By 7 days after tumor in inoculation, up to 18% of the spleen cells were producing virus yielding greater than 10(8) plaque-forming units per spleen. Similarly, P815 cells induced the viral-permissive state in allogeneic C3H/HeN mice. Tumors other than P815 were also effective in permitting VSV growth in the spleen. The presence of tumor cells themselves was not sufficient for VSV growth, yet cell-free ascitic fluid from mice bearing syngeneic tumors inoculated 3 h before infection allowed for VSV replication. Cell-free supernatant from a T-cell hybridoma synthesizing interleukin-2 was also effective in permitting virus growth when inoculated 3 h before infection. The virus-permissive cell has been characterized as a nylon wool-adherent and plastic dish-nonadherent spleen cell.