A New Anti HIV/AIDS Strategy: Possible Chemical Induction of Endogenous Type 1 Interferon

A. Achour
{"title":"A New Anti HIV/AIDS Strategy: Possible Chemical Induction of Endogenous Type 1 Interferon","authors":"A. Achour","doi":"10.2174/1876518101002010084","DOIUrl":null,"url":null,"abstract":"Aids is characterized by progressive T cell depletion, immune cells dysfunctions and interferon responsiveness that are driven by chronic activation. Antiretroviral therapy (ART), although effective in improving the survival of HIV-1- infected individuals, has not been able to reconstitute the adaptive immunity. However, ART is neither able to eradicate the virus nor has sufficient immune-modulatory effects to control viral infection. This situation points out the dilemma that current HIV therapy can maintain the disease in a resting state, but not eliminate it. We have described the use of novel chemical agents able to restore T-cell survival by inducing cytokines production. More recently, we suggested a complementary therapy based on the chemical induction of endogenous  / interferon. We suggest that a therapeutic strategy based upon chemical immune restoration associated with type 1 Interferon (IFN- / ) might represent a mean for HIV cure. This finding may be vital for future therapeutic approaches in AIDS disease and the immune reconstitution. Understanding these process can lead to a range of new therapeutic interventions.","PeriodicalId":22920,"journal":{"name":"The Open Antimicrobial Agents Journal","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2010-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Open Antimicrobial Agents Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1876518101002010084","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Aids is characterized by progressive T cell depletion, immune cells dysfunctions and interferon responsiveness that are driven by chronic activation. Antiretroviral therapy (ART), although effective in improving the survival of HIV-1- infected individuals, has not been able to reconstitute the adaptive immunity. However, ART is neither able to eradicate the virus nor has sufficient immune-modulatory effects to control viral infection. This situation points out the dilemma that current HIV therapy can maintain the disease in a resting state, but not eliminate it. We have described the use of novel chemical agents able to restore T-cell survival by inducing cytokines production. More recently, we suggested a complementary therapy based on the chemical induction of endogenous  / interferon. We suggest that a therapeutic strategy based upon chemical immune restoration associated with type 1 Interferon (IFN- / ) might represent a mean for HIV cure. This finding may be vital for future therapeutic approaches in AIDS disease and the immune reconstitution. Understanding these process can lead to a range of new therapeutic interventions.
一种新的抗HIV/AIDS策略:内源性1型干扰素可能的化学诱导
艾滋病的特点是进行性T细胞耗竭、免疫细胞功能障碍和干扰素反应,这些都是由慢性激活驱动的。抗逆转录病毒疗法(ART)虽然能有效地改善HIV-1感染者的生存,但不能重建适应性免疫。然而,抗逆转录病毒治疗既不能根除病毒,也没有足够的免疫调节作用来控制病毒感染。这种情况指出了目前的艾滋病治疗只能使疾病处于静止状态,而不能消除它的困境。我们已经描述了能够通过诱导细胞因子产生来恢复t细胞存活的新型化学制剂的使用。最近,我们提出了一种基于内源性/干扰素化学诱导的补充疗法。我们建议一种基于化学免疫恢复的治疗策略,与1型干扰素(IFN-/)相关,可能代表一种治愈HIV的方法。这一发现可能对未来艾滋病疾病的治疗方法和免疫重建至关重要。了解这些过程可以导致一系列新的治疗干预措施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信