Schwartzberg表示，这一新方法并不能够为HIV疫苗的研发提供希望。这应该是一种帮助已经感染了HIV的人的策略，而不是一种预防措施。（科学网 梅进/编译）
原始出处：（PNAS），doi：10.1073/pnas.0709659105，Julie A. Readinger，Pamela L. Schwartzberg Selective targeting of ITK blocks multiple steps of HIV replication
Julie A. Readinger*, Gillian M. Schiralli{dagger},{ddagger}, Jian-Kang Jiang§,¶, Craig J. Thomas§,¶, Avery August{dagger}, Andrew J. Henderson{dagger},{ddagger},||, and Pamela L. Schwartzberg*,||
Abstract
Treatment for HIV has relied on the use of antiretroviral agents that can be subject to the development of resistant viruses. The study of inhibitors directed against cellular proteins required for HIV replication is therefore of growing interest. Inducible T cell kinase (ITK) is a Tec family tyrosine kinase that regulates T cell receptor (TCR)-induced activation of PLC{gamma}-1, Ca2+ mobilization and transcription factor activation, and actin rearrangement downstream of both TCR and chemokine receptors. Because productive infection of T cells with HIV requires T cell activation, chemokine receptors and actin reorganization, we asked whether ITK affects HIV infection using ITK-specific siRNA, a kinase-inactive ITK mutant or an ITK inhibitor. We demonstrate that loss of ITK function resulted in marked reductions in intracellular p24 levels upon HIV infection. Loss of ITK function after establishment of HIV infection also decreased virus spread within the culture. Inhibition of ITK did not affect expression of the HIV coreceptors CD4 or CXCR4 but partially blocked HIV viral entry, an effect that correlated with decreased actin polarization to gp120. Additionally, ITK was required for efficient HIV transcription, and overexpression of ITK increased both viral transcription and virus-like particle formation. Our data suggest that inhibition of ITK blocks HIV infection by affecting multiple steps of HIV replication.
美国研究人员２８日公布的研究结果显示，人体中一种蛋白质失去活性后有助于抵抗艾滋病病毒。这一重要发现为防治艾滋病带来新希望。