|本期目录/Table of Contents|

[1]周明菊,李 静,张和倩,等.HIV 病毒库清除策略中潜伏逆转剂的应用及挑战[J].传染病信息,2018,06:511-515.
 ZHOU Ming-ju,LI Jing,ZHANG He-qian,et al.Application and challenges of latent reversal agent in elimination strategy of latent HIV reservoir[J].Infectious Disease Information,2018,06:511-515.
点击复制

HIV 病毒库清除策略中潜伏逆转剂的应用及挑战(PDF)

《传染病信息》[ISSN:1007-8134/CN:11-3886/R]

期数:
2018年06期
页码:
511-515
栏目:
导向与述评
出版日期:
2018-12-30

文章信息/Info

Title:
Application and challenges of latent reversal agent in elimination strategy of latent HIV reservoir
作者:
周明菊李 静张和倩靳婕华宋锦文张 超王福生
233000,蚌埠医学院临床系(周明菊、李静、张和倩、 王福生);100039 北京,中国人民解放军总医院第五医学中心感 染性疾病诊疗与研究中心(靳婕华、宋锦文、张超、王福生)
Author(s):
ZHOU Ming-ju LI Jing ZHANG He-qian JIN Jie-hua SONG Jin-wen ZHANG Chao* WANG Fu-sheng*
Department of Clinical Medicine, Bengbu Medical College, 233000, China
关键词:
艾滋病激活和清除潜伏病毒库潜伏逆转剂
Keywords:
AIDS Shock and Kill latent reservoir latency-reversing agent
分类号:
R512.91
DOI:
10.3969/j.issn.1007-8134.2018.06.004
文献标识码:
A
摘要:
高效抗反转录病毒治疗能够有效抑制HIV 复制,但患者须终身服药且不能清除病毒库。通过激活和清除策略 有望彻底清除病毒库。本文对潜伏逆转剂及潜伏病毒库清除策略的基础及临床研究的进展进行综述。 
Abstract:
Despite the success of highly active antiretroviral therapy in suppressing HIV replication, treatment is lifelong and it cannot completely eliminate latent reservoir. “Shock and Kill’’ strategy is potential for purging the reservoir of HIV. This paper reviews the progress on basic and clinical studies in latency-reversing agent and the elimination strategy of latent reservior.     

参考文献/References


[1] Kim Y, Anderson JL, Lewin SR. Getting the “Kill” into “Shock and Kill”: strategies to eliminate latent HIV[J]. Cell Host Microbe, 2018, 23(1):14-26.
[2] Henrich TJ, Hatano H, Bacon O, et al. HIV-1 persistence following extremely early initiation of antiretroviral therapy (ART) during acute HIV-1 infection: an observational study[J]. PLoS Med, 2017, 14(11):e1002417.
[3] Bruner KM, Murray AJ, Pollack RA, et al. Defective proviruses rapidly accumulate during acute HIV-1 infection[J]. Nat Med, 2016, 22(9):1043-1049.
[4] Eriksson S, Graf EH, Dahl V, et al. Comparative analysis of measures of viral reservoirs in HIV-1 eradication studies[J]. PLoS Pathog, 2013, 9(2):e1003174.
[5] Ho YC, Shan L, Hosmane NN, et al. Replication-competent noninduced proviruses in the latent reservoir increase barrier to HIV-1 cure[J]. Cell, 2013, 155(3):540-551.
[6] Hosmane NN, Kwon KJ, Bruner KM, et al. Proliferation of latently 传染病信息 2018 年12 月30 日 第31 卷 第6 期 Infect Dis Info, Vol. 31, No. 6, December 30, 2018 ·515· infected CD4(+) T cells carrying replication-competent HIV-1: potential role in latent reservoir dynamics[J]. J Exp Med, 2017, 214(4):959-972.
[7] Archin NM, Liberty AL, Kashuba AD, et al. Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy[J]. Nature, 2012, 487(7408):482-485.
[8] Elliott JH, Wightman F, Solomon A, et al. Activation of HIV transcription with short-course vorinostat in HIV-infected patients on suppressive antiretroviral therapy[J]. PLoS Pathog, 2014, 10(10):e1004473.
[9] Archin NM, Kirchherr JL, Sung JA, et al. Interval dosing with the HDAC inhibitor vorinostat effectively reverses HIV latency[J]. J Clin Invest, 2017, 127(8):3126-3135.
[10] Sogaard OS, Graversen ME, Leth S, et al. The depsipeptide romidepsin reverses HIV-1 latency in vivo[J]. PLoS Pathog, 2015, 11(9):e1005142.
[11] Rasmussen TA, Tolstrup M, Brinkmann CR, et al. Panobinostat, a histone deacetylase inhibitor, for latent-virus reactivation in HIVinfected patients on suppressive antiretroviral therapy: a phase 1/2, single group, clinical trial[J]. Lancet HIV, 2014, 1(1):e13-e21.
[12] Gutierrez C, Serrano-Villar S, Madrid-Elena N, et al. Bryostatin-1 for latent virus reactivation in HIV-infected patients on antiretroviral therapy[J]. AIDS, 2016, 30(9):1385-1392.
[13] Spivak AM, Andrade A, Eisele E, et al. A pilot study assessing the safety and latency-reversing activity of disulfiram in HIV- 1-infected adults on antiretroviral therapy[J]. Clin Infect Dis, 2014, 58(6):883-890.
[14] Elliott JH, Mcmahon JH, Chang CC, et al. Short-term administration of disulfiram for reversal of latent HIV infection: a phase 2 dose-escalation study[J]. Lancet HIV, 2015, 2(12):e520-e529.
[15] Vibholm L, Schleimann MH, Hojen JF, et al. Short-course Tolllike receptor 9 agonist treatment impacts innate immunity and plasma viremia in individuals with human immunodeficiency virus infection[J]. Clin Infect Dis, 2017, 64(12):1686-1695.
[16] Blazkova J, Trejbalova K, Gondois-Rey F, et al. CpG methylation controls reactivation of HIV from latency[J]. PLoS Pathog, 2009, 5(8):e1000554.
[17] Bouchat S, Gatot JS, Kabeya K, et al. Histone methyltransferase inhibitors induce HIV-1 recovery in resting CD4(+) T cells from HIV-1-infected HAART-treated patients[J]. AIDS, 2012, 26(12):1473-1482.
[18] Pitman MC, Lau JSY, Mcmahon JH, et al. Barriers and strategies to achieve a cure for HIV[J]. Lancet HIV, 2018, 5(6):e317-e328.
[19] Tahirov TH, Babayeva ND, Varzavand K, et al. Crystal structure of HIV-1 Tat complexed with human P-TEFb[J]. Nature, 2010, 465(7299):747-751.
[20] Boehm D, Calvanese V, Dar RD, et al. BET bromodomain-targeting compounds reactivate HIV from latency via a Tat-independent mechanism[J]. Cell Cycle, 2013, 12(3):452-462.
[21] Zhang XX, Lin J, Liang TZ, et al. The BET bromodomain inhibitor apabetalone induces apoptosis of latent HIV-1 reservoir cells following viral reactivation[J]. Acta Pharmacol Sin, 2018. doi:10.1038/s41401-018-0027-5.
[22] Jiang G, Nguyen D, Archin NM, et al. HIV latency is reversed by ACSS2-driven histone crotonylation[J]. J Clin Invest, 2018, 128(3):1190-1198.
[23] Brogdon J, Ziani W, Wang X, et al. In vitro effects of the smallmolecule protein kinase C agonists on HIV latency reactivation[J]. Sci Rep, 2016, 6:39032.
[24] Tsai A, Irrinki A, Kaur J, et al. Toll-like receptor 7 agonist GS- 9620 induces HIV expression and HIV-specific immunity in cells from HIV-infected individuals on suppressive antiretroviral therapy [J]. J Virol, 2017, 91(8):e02166-16.
[25] Doyon G, Zerbato J, Mellors JW, et al. Disulfiram reactivates latent HIV-1 expression through depletion of the phosphatase and tensin homolog[J]. AIDS, 2013, 27(2):F7-F11.
[26] Das B, Dobrowolski C, Luttge B, et al. Estrogen receptor-1 is a key regulator of HIV-1 latency that imparts gender-specific restrictions on the latent reservoir[J]. Proc Natl Acad Sci U S A, 2018, 115(33):e7795-e7804.
[27] Battivelli E, Dahabieh MS, Abdel-Mohsen M, et al. Distinct chromatin functional states correlate with HIV latency reactivation in infected primary CD4(+) T cells[J]. Elife, 2018, 7:e34655.
[28] Clutton GT, Jones RB. Diverse impacts of HIV latency-reversing agents on CD8+ T-cell function: implications for HIV cure[J]. Front Immunol, 2018, 9:1452.
[29] Leth S, Schleimann MH, Nissen SK, et al. Combined effect of Vacc-4x, recombinant human granulocyte macrophage colonystimulating factor vaccination, and romidepsin on the HIV-1 reservoir (REDUC): a single-arm, phase 1B/2A trial[J]. Lancet HIV, 2016, 3(10):e463-e472.
[30] Hansen SG, Ford JC, Lewis MS, et al. Profound early control of highly pathogenic SIV by an effector memory T-cell vaccine[J]. Nature, 2011, 473(7348):523-527.
[31] Borducchi EN, Cabral C, Stephenson KE, et al. Ad26/MVA therapeutic vaccination with TLR7 stimulation in SIV-infected rhesus monkeys[J]. Nature, 2016, 540(7632):284-287.
[32] Kong R, Xu K, Zhou T, et al. Fusion peptide of HIV-1 as a site of vulnerability to neutralizing antibody[J]. Science, 2016, 352(6287):828-833.
[33] Sung JA, Pickeral J, Liu L, et al. Dual-Affinity Re-Targeting proteins direct T cell-mediated cytolysis of latently HIV-infected cells[J]. J Clin Invest, 2015, 125(11):4077-4090.
[34] Pollack RA, Jones RB, Pertea M, et al. Defective HIV-1 proviruses are expressed and can be recognized by cytotoxic T lymphocytes, which shape the proviral landscape[J]. Cell Host Microbe, 2017, 21(4):494-506.
[35] Banga R, Procopio FA, Noto A, et al. PD-1(+) and follicular helper T cells are responsible for persistent HIV-1 transcription in treated aviremic individuals[J]. Nat Med, 2016, 22(7):754-761.
[36] Descours B, Petitjean G, Lopez-Zaragoza JL, et al. CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replicationcompetent proviruses[J]. Nature, 2017, 543(7646):564-567.
[37] Bertagnolli LN, White JA, Simonetti FR, et al. The role of CD32 during HIV-1 infection[J]. Nature, 2018, 561(7723):e17-e19.
[38] Byrareddy SN, Kallam B, Arthos J, et al. Targeting alpha4beta7 integrin reduces mucosal transmission of simian immunodeficiency virus and protects gut-associated lymphoid tissue from infection[J]. Nat Med, 2014, 20(12):1397-1400.
[39] Guzzo C, Ichikawa D, Park C, et al. Virion incorporation of integrin alpha4beta7 facilitates HIV-1 infection and intestinal homing[J]. Sci Immunol, 2017, 2(11):eaam7341.
[40] Gay CL, Bosch RJ, Ritz J, et al. Clinical trial of the Anti- PD-L1 antibody BMS-936559 in HIV-1 infected participants on suppressive antiretroviral therapy[J]. J Infect Dis, 2017, 215(11):1725-1733.
[41] He R, Hou S, Liu C, et al. Follicular CXCR5- expressing CD8(+) T cells curtail chronic viral infection[J]. Nature, 2016, 537(7620):412-428.
[42] Zhang Z, Fu J, Xu X, et al. Safety and immunological responses to human mesenchymal stem cell therapy in difficult-to-treat HIV- 1-infected patients[J]. AIDS, 2013, 27(8):1283-1293.
[43] Wang FS, Zhang L, Douek D, et al. Strategies for an HIV cure: progress and challenges[J]. Nat Immunol, 2018, 19(11):1155- 1158.

备注/Memo

备注/Memo:
[ 基金项目] 首都特色基金 (Z161100000516011)
[ 作者单位] 233000,蚌埠医学院临床系(周明菊、李静、张和倩、 王福生);100039 北京,中国人民解放军总医院第五医学中心感 染性疾病诊疗与研究中心(靳婕华、宋锦文、张超、王福生)
[ 通信作者] 张超,E-mail: zhangch302@163.com;王福生,E-mail: fswang302@163.com
更新日期/Last Update: 2018-12-30