Mechanisms of pathogenesis induced by bovine leukemia virus as a model for human T-cell leukemia virus.
Mechanisms of pathogenesis induced by bovine leukemia virus as a model for human T-cell leukemia virus.
复制标题
DOI：
10.3389/fmicb.2013.00328
复制
发表时间：
2013
影响因子：
5.2
通讯作者：
Takeshima SN
中科院分区：
文献类型：
--
作者：
Aida Y;Murakami H;Takahashi M;Takeshima SN
牛白血病病毒（BLV）和人T细胞白血病病毒1型（HTLV-1）组成了一个独特的逆转录病毒家族。这两种病毒均诱导慢性淋巴组织增生性疾病，其中BLV影响B细胞谱系，HTLV-1影响T细胞谱系。BLV和HTLV诱导的感染的病理学非常相似，不存在慢性病毒血症和长潜伏期。这些病毒在位于env基因和3′长末端重复序列之间的pX区编码至少两种调节蛋白，即Tax和雷克斯。Tax蛋白是病毒致癌潜力的关键贡献者，也是参与病毒复制的关键蛋白。然而，BLV感染不足以导致白血病发生，还必须发生其他事件，如基因突变。在这篇综述中，我们首先总结了两种病毒在基因组组织，病毒学和病理学方面的相似之处。然后，我们描述了BLV模型的当前知识，这也可能是相关的理解由HTLV-1引起的白血病。此外，我们通过新鉴定的BLV Tax突变体解决了我们对Tax功能的更好理解，这些突变体在氨基酸240和265之间具有取代。
Bovine leukemia virus (BLV) and human T-cell leukemia virus type 1 (HTLV-1) make up a unique retrovirus family. Both viruses induce chronic lymphoproliferative diseases with BLV affecting the B-cell lineage and HTLV-1 affecting the T-cell lineage. The pathologies of BLV- and HTLV-induced infections are notably similar, with an absence of chronic viraemia and a long latency period. These viruses encode at least two regulatory proteins, namely, Tax and Rex, in the pX region located between the env gene and the 3′ long terminal repeat. The Tax protein is a key contributor to the oncogenic potential of the virus, and is also the key protein involved in viral replication. However, BLV infection is not sufficient for leukemogenesis, and additional events such as gene mutations must take place. In this review, we first summarize the similarities between the two viruses in terms of genomic organization, virology, and pathology. We then describe the current knowledge of the BLV model, which may also be relevant for the understanding of leukemogenesis caused by HTLV-1. In addition, we address our improved understanding of Tax functions through the newly identified BLV Tax mutants, which have a substitution between amino acids 240 and 265.
登录
查看更多内容
影响因子：
3.3
作者：
Boxus M;Twizere JC;Legros S;Dewulf JF;Kettmann R;Willems L
通讯作者：
Willems L
影响因子：
2.1
作者：
Bangham, CRM
通讯作者：
Bangham, CRM
影响因子：
5.4
作者：
ADAM, E;KERKHOFS, P;WILLEMS, L
通讯作者：
WILLEMS, L
影响因子：
20.3
作者：
Andresen, Vibeke;Pise-Masison, Cynthia A.;Franchini, Genoveffa
通讯作者：
Franchini, Genoveffa
影响因子：
5.4
作者：
DERSE, D
通讯作者：
DERSE, D