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在小鼠中由弗氏病毒诱导的红白血病进展过程中病毒合成的停止。

Shut-down of virus synthesis during progression of erythroleukemia induced by Friend virus in mice.

作者信息

Yoosook C

出版信息

Int J Cancer. 1982 Jun 15;29(6):659-65. doi: 10.1002/ijc.2910290610.

Abstract

Infection of (C57BL/6 X DBA/2)F1 (BDF1) mice with 2,500 FFU of Friend virus complex (FV) resulted in erythroleukemia followed by recovery, at which time virus could not be detected in the spleens of mice, and with splenomegaly (progressor mice) or without splenomegaly (regressor mice). Progressor and regressor mice developed equally high amounts of FV-neutralizing activity in their sera. Progressor mice contained cells capable of producing virus, despite the lack of viral envelope antigen(s) in their spleens. The tropism of FV recoverable from the spleens of secondary recipients, injected with spleen cells from progressor mice, did not show any change, although the viral genome was present in Fv-I-restrictive host for at least 7 weeks. When the number of spleen colony-generating cells was enumerated, by the spleen colony assay, the frequency in normal syngeneic and in allogeneic hosts was approximately the same at the early stage of erythroleukemia but was about 1,000 times higher in the syngeneic recipients during leukemia progression. These spleen colony-generating cells were considered to be FV-transformed cells capable of self-renewal and capable of generating infectious centers (IC), respectively. Most of these transformed cells might be non-producer leukemia cells.

摘要

用2500个蚀斑形成单位(FFU)的弗氏病毒复合物(FV)感染(C57BL/6×DBA/2)F1(BDF1)小鼠,会导致红白血病,随后恢复,此时在小鼠脾脏中检测不到病毒,并且会出现脾肿大(进展型小鼠)或无脾肿大(回归型小鼠)。进展型和回归型小鼠血清中产生的FV中和活性水平相当。尽管进展型小鼠脾脏中缺乏病毒包膜抗原,但仍含有能够产生病毒的细胞。从接受了进展型小鼠脾细胞注射的二次受体脾脏中回收的FV嗜性没有任何变化,尽管病毒基因组在Fv-I限制型宿主中存在了至少7周。通过脾集落试验对脾集落生成细胞数量进行计数时,在红白血病早期,正常同基因宿主和异基因宿主中的频率大致相同,但在白血病进展期间,同基因受体中的频率约高1000倍。这些脾集落生成细胞分别被认为是能够自我更新和能够产生感染中心(IC)的FV转化细胞。这些转化细胞中的大多数可能是非生产性白血病细胞。

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