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外源性和内源性白血病病毒基因——综述

Exogenous and endogenous leukosis virus genes--a review.

作者信息

Crittenden L B

机构信息

U.S. Department of Agriculture, Science and Education Administration, Agricultural Research, Regional Poultry Research Laboratory, East Lansing, Michigan 48823, USA.

出版信息

Avian Pathol. 1981 Apr;10(2):101-12. doi: 10.1080/03079458108418464.

Abstract

Lymphoid leukosis is induced by exogenous retroviruses (LLV) that replicate via a DNA intermediate that is integrated into host somatic cell DNA. Variation in endogenous LLV expression is largely controlled by location of DNA proviruses integrated in the host germ-line and inherited as Mendelian genes. Present evidence suggests that endogenous viral genes (ev loci) arose from germ-line integration of exogenous LLVs and that those integrated ev loci expressing high levels of virus are at a selective disadvantage. Exogenous LLV infection leads not only to development of LL in some chickens but also to reduced productivity of layers. Results of preliminary experiments suggest that variation in ev locus expression influences non-oncogenic pathology and immune response after infection with an LLV known to be structurally related to ev loci. The effect of these loci on response to infection by unrelated micro organisms and on productivity should now be studied to determine whether the breeder should be concerned with these genes.

摘要

淋巴细胞白血病由外源性逆转录病毒(LLV)诱导,这些病毒通过整合到宿主体细胞DNA中的DNA中间体进行复制。内源性LLV表达的变异在很大程度上受整合到宿主种系中的DNA前病毒位置控制,并作为孟德尔基因遗传。目前的证据表明,内源性病毒基因(ev位点)起源于外源性LLV的种系整合,而那些表达高水平病毒的整合ev位点处于选择劣势。外源性LLV感染不仅会导致一些鸡发生淋巴细胞白血病,还会降低蛋鸡的生产力。初步实验结果表明,ev位点表达的变异会影响感染与ev位点结构相关的LLV后的非致癌病理和免疫反应。现在应该研究这些位点对感染无关微生物的反应以及对生产力的影响,以确定育种者是否应该关注这些基因。

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