REPLICATION OF VESICULAR STOMATITIS-VIRUS IN MOUSE SPLEEN-CELLS
REPLICATION OF VESICULAR STOMATITIS-VIRUS IN MOUSE SPLEEN-CELLS
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DOI：
10.1128/iai.32.3.1014-1023.1981
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发表时间：
1981-01-01
影响因子：
3.1
通讯作者：
PAUL, WE
中科院分区：
文献类型：
--
作者：
HECHT, TT;PAUL, WE
小鼠脾细胞通常不能支持水泡性口炎病毒(VSV)的体内复制，但在腹腔注射后，小鼠脾细胞对VSV感染变得易感。某些同基因和同种异体肿瘤的生长。P815肿瘤细胞在同基因DBA/2小鼠体内生长3天后，建立了VSV复制的病毒允许状态。在肿瘤接种后7天，高达18%的脾细胞产生病毒，每个脾产生108个空斑形成单位。同样，P815细胞在同种异体C3H/HEN小鼠中诱导了病毒允许状态。P815以外的其他肿瘤也有效地促进了VSV在脾内的生长。肿瘤细胞本身的存在不足以使VSV生长，但在感染前3h接种来自同基因肿瘤小鼠的无细胞腹水允许VSV复制。合成IL-2的T细胞杂交瘤的无细胞培养上清液在感染前3h接种也能有效地促进病毒的生长。病毒允许细胞的特征是尼龙羊毛贴壁和塑料培养皿不贴壁的脾细胞。
Mouse spleen cells which normally cannot support the in vivo replication of vesicular stomatitis virus (VSV) became susceptible to VSV infection after the i.p. 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 was established. By 7 days after tumor inoculation, up to 18% of the spleen cells were producing virus yielding > 108 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 was characterized as a nylon wool-adherent and plastic dish-nonadherent spleen cell.