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Diminished potential for B-lymphoid differentiation after murine leukemia virus infection in vivo and in EML hematopoietic progenitor cells.在体内以及EML造血祖细胞中，小鼠白血病病毒感染后B淋巴细胞分化潜能降低。
J Virol. 2007 Jul;81(13):7274-9. doi: 10.1128/JVI.00250-07. Epub 2007 Apr 11.
2
Substitution of feline leukemia virus long terminal repeat sequences into murine leukemia virus alters the pattern of insertional activation and identifies new common insertion sites.将猫白血病病毒长末端重复序列替换到鼠白血病病毒中会改变插入激活模式并识别出新的常见插入位点。
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本文引用的文献

1
Genetic networks that regulate B lymphopoiesis.调节B淋巴细胞生成的基因网络。
Curr Opin Hematol. 2005 May;12(3):203-9. doi: 10.1097/01.moh.0000160735.67596.a0.
2
Unique long terminal repeat and surface glycoprotein gene sequences of feline leukemia virus as determinants of disease outcome.猫白血病病毒独特的长末端重复序列和表面糖蛋白基因序列作为疾病转归的决定因素。
J Virol. 2005 May;79(9):5278-87. doi: 10.1128/JVI.79.9.5278-5287.2005.
3
Subtle mutational changes in the SU protein of a natural feline leukemia virus subgroup A isolate alter disease spectrum.一株天然的A型猫白血病病毒分离株的SU蛋白中细微的突变变化改变了疾病谱。
J Virol. 2005 Feb;79(3):1351-60. doi: 10.1128/JVI.79.3.1351-1360.2005.
4
Substitution of feline leukemia virus long terminal repeat sequences into murine leukemia virus alters the pattern of insertional activation and identifies new common insertion sites.将猫白血病病毒长末端重复序列替换到鼠白血病病毒中会改变插入激活模式并识别出新的常见插入位点。
J Virol. 2005 Jan;79(1):57-66. doi: 10.1128/JVI.79.1.57-66.2005.
5
In vitro selective suppression of feline myeloid colony formation is attributable to molecularly cloned strain of feline leukemia virus with unique long terminal repeat.体外对猫骨髓集落形成的选择性抑制归因于具有独特长末端重复序列的分子克隆猫白血病病毒株。
Res Vet Sci. 2005 Apr;78(2):151-4. doi: 10.1016/j.rvsc.2004.07.003.
6
Feline leukaemia virus LTR variation and disease association in a geographical and temporal cluster.猫白血病病毒长末端重复序列变异与地理和时间集群中的疾病关联
J Gen Virol. 2004 Oct;85(Pt 10):2937-2942. doi: 10.1099/vir.0.80149-0.
7
The roles of transcription factors in B lymphocyte commitment, development, and transformation.转录因子在B淋巴细胞定向分化、发育及转化过程中的作用。
J Leukoc Biol. 2004 Jun;75(6):973-81. doi: 10.1189/jlb.1103554. Epub 2004 Feb 24.
8
Cooperation between IL-7 and the pre-B cell receptor: a key to B cell selection.白细胞介素-7与前B细胞受体之间的合作：B细胞选择的关键
Semin Immunol. 2002 Dec;14(6):423-30. doi: 10.1016/s1044532302000775.
9
Roles of EBF and Pax-5 in B lineage commitment and development.早期B细胞因子（EBF）和配对盒蛋白5（Pax-5）在B淋巴细胞定向分化及发育中的作用。
Semin Immunol. 2002 Dec;14(6):415-22. doi: 10.1016/s1044532302000763.
10
Mapping gene expression patterns during myeloid differentiation using the EML hematopoietic progenitor cell line.利用EML造血祖细胞系绘制髓系分化过程中的基因表达模式。
Exp Hematol. 2002 Jul;30(7):649-58. doi: 10.1016/s0301-472x(02)00817-2.

在体内以及EML造血祖细胞中，小鼠白血病病毒感染后B淋巴细胞分化潜能降低。

Diminished potential for B-lymphoid differentiation after murine leukemia virus infection in vivo and in EML hematopoietic progenitor cells.

作者信息

Finstad Samantha L, Rosenberg Naomi, Levy Laura S

机构信息

Department of Microbiology and Immunology, Tulane University School of Medicine, 1430 Tulane Avenue SL-38, New Orleans, LA 70112, USA.

出版信息

J Virol. 2007 Jul;81(13):7274-9. doi: 10.1128/JVI.00250-07. Epub 2007 Apr 11.

DOI:10.1128/JVI.00250-07
PMID:17428873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1933319/
Abstract

Infection with a recombinant murine-feline gammaretrovirus, MoFe2, or with the parent virus, Moloney murine leukemia virus, caused significant reduction in B-lymphoid differentiation of bone marrow at 2 to 8 weeks postinfection. The suppression was selective, in that myeloid potential was significantly increased by infection. Analysis of cell surface markers and immunoglobulin H gene rearrangements in an in vitro model demonstrated normal B-lymphoid differentiation after infection but significantly reduced viability of differentiating cells. This reduction in viability may confer a selective advantage on undifferentiated lymphoid progenitors in the bone marrow of gammaretrovirus-infected animals and thereby contribute to the establishment of a premalignant state.

摘要

感染重组鼠-猫γ逆转录病毒MoFe2或其亲本病毒莫洛尼鼠白血病病毒，在感染后2至8周会导致骨髓B淋巴细胞分化显著减少。这种抑制具有选择性，因为感染会使髓系潜能显著增加。在体外模型中对细胞表面标志物和免疫球蛋白H基因重排的分析表明，感染后B淋巴细胞分化正常，但分化细胞的活力显著降低。这种活力降低可能赋予γ逆转录病毒感染动物骨髓中未分化淋巴祖细胞选择性优势，从而有助于建立癌前状态。