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在体外感染富含祖细胞的恒河猴骨髓(BM)中,猿猴免疫缺陷病毒(SIV)的恢复及集落形成的抑制。

Recovery of the simian immunodeficiency virus (SIV) and depression of colony formation in in vitro infected progenitor cell-enriched rhesus bone marrow (BM).

作者信息

Beltz L, Narayan O, Adams R J, Noga S J, Donnenberg A D

机构信息

Oncology Center, School of Medicine, Johns Hopkins University, Baltimore, MD.

出版信息

J Med Primatol. 1991 Jun;20(4):144-51.

PMID:1942003
Abstract

Rhesus progenitor-enriched BM was exposed overnight to SIV and cultured in a limiting dilution assay where the potential for progenitor interaction with lymphocytes or macrophages was low. Virus was consistently isolated late in culture, detection being aided by coculture with CEM174 lymphoblasts. Although infected cells had reduced clonogenic activity, colonies were indistinguishable from those derived from uninfected BM with respect to proliferative potential, morphology, and longevity in culture. Primate immunodeficiency viruses, therefore, may infect immature BM populations, directly affecting hematopoietic activity.

摘要

富含恒河猴祖细胞的骨髓与猴免疫缺陷病毒(SIV)接触过夜,并在有限稀释分析中进行培养,在该分析中祖细胞与淋巴细胞或巨噬细胞相互作用的可能性较低。病毒在培养后期始终能够被分离出来,通过与CEM174淋巴母细胞共培养有助于检测。尽管受感染的细胞克隆形成活性降低,但就增殖潜力、形态和培养中的寿命而言,这些集落与未感染骨髓来源的集落无法区分。因此,灵长类免疫缺陷病毒可能感染未成熟的骨髓群体,直接影响造血活性。

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