生物专业英语翻译，，，急啊

Viral proteins and cellular partners involved in the
early events in the emergence of HIV from latency to
active replication have been a focus of drug development,
because the problems associated with both
emergence of viral resistance and perturbation of cellular
metabolism as well as viral knockdown vastly increase
after the onset of active HIV replication. The Tat–TAR
interaction has received special attention due to its
central role in the HIV transcriptional transactivation,
but cellular cofactors such as NF-kB are also targets of
drug development.4 Not surprisingly, drugs against
cellular cofactors have high toxicity, but are still being
pursued as options in the event of failure of HAART
chemotherapy. Other recently identified cofactors in
activation of HIV transcription include the Werner’s
syndrome helicase5 and p90 ribosomal S6 kinase 2
(RSK2).6
There has also been a great deal of interest re

病毒在介入的蛋白质和多孔的伙伴 在HIV诞生的early事件从潜伏的
active复制是药物发展， 焦点 问题联系两个的because 多孔的的病毒抵抗和扰动emergence 并且病毒浩大击倒增量的metabolismafter活跃HIV复制起始。 Tat–TAR
interaction接受了特别留意由于它的在HIV transcriptional transactivation的central角色，
but多孔的辅助因素例如NF千字节也是的目标drug development.4毫不奇怪，药物反对
cellular辅助因素有高毒力，但是仍然是作为选择的pursued在HAART情形下的失败
chemotherapy. 其他最近辨认的辅助因素 HIV副本的activation包括Werner’s
syndrome helicase5和p90核醣体的S6激酶2
(RSK2) .6
There也是关于的很多兴趣the沥青束缚的蛋白质(TRBP)和它的对HIV 的作用replication. TRBP最初被辨认了作为活化计
of HIV副本，它的随后公认作为Dicer7 partner导致了建议沥青推翻
the核糖核酸在HIV期间的干涉(RNAi)路
infection通过隔离TRBP，是的8 导致的expected在内在的全球性减退
microRNA水平。 然而，在两的HIV感染症结果具体多孔的microRNAs.9 的up-和downregulationTRBP siRNA-mediated击倒减少表示
of RT和HIV在海拉细胞的总蛋白含量水平 与pNL4-3 proviral脱氧核糖核酸的transfected，当肌动蛋白成水平时未受影响的are，建议TRBP主要地行动这与是一致的to激活HIV replication.10observations TRBP低内在表示是
directly与在星形细胞的低HIV复制和连接了TRBP increasing表示在astrocytoma细胞的 对水平的increases病毒复制和被观察的一样in海拉cells.11， 12 TRBP被认为增加HIV