生物专业英语翻译，，，急啊

Question

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 regarding
the TAR-binding protein (TRBP) and its effects on HIV
replication. TRBP was initially identified as an activator
of HIV transcription, its subsequent recognition as a
partner of Dicer7 led to the suggestion that TAR subverts
the RNA interference (RNAi) pathway during HIV
infection by sequestering TRBP,8 which would be
expected to lead to a global decrease in endogenous
microRNA levels. However, HIV infection results in both
up- and downregulation of specific cellular microRNAs.9
siRNA-mediated knockdown of TRBP decreases expression
of RT and HIV total protein levels in HeLa cells
transfected with pNL4-3 proviral DNA while actin levels
are unaffected, suggesting that TRBP acts predominantly
to activate HIV replication.10 This is consistent with
observations that low endogenous expression of TRBP is
directly linked to low HIV replication in astrocytes, and
increasing expression of TRBP in astrocytoma cells
increases viral replication to the same level as observed
in HeLa cells.11,12 TRBP is thought to increase HIV
replication through its known effect as an antagonist to
PKR (RNA-binding protein kinase), inhibiting PKR
activation of the cellular immune response.
Additional cellular factors involved in HIV replication
continue to be identified. These include 11 cellular
microRNAs that are upregulated and downregulated9

Answer 1

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
replication通过它作为一个反对者的已知的作用的PKR (核糖核酸束缚的蛋白激酶)，禁止的PKR 多孔的免疫反应的activation。 在HIV复制介入的Additional多孔的因素将被辨认的continue。 这些包括11多孔 upregulated和downregulated9的microRNAs