Host factors regulating post-integration latency of HIV

被引：37

作者：

Williams, SAF

Greene, WC ^{[1
]}

机构：

[1] Univ Calif San Francisco, Dept Med Microbiol & Immunol, San Francisco, CA 94143 USA

[2] Gladstone Inst Virol & Immunol, San Francisco, CA 94158 USA

[3] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA

来源：

TRENDS IN MICROBIOLOGY | 2005年 / 13卷 / 04期

关键词：

D O I：

10.1016/j.tim.2005.02.006

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A recent study has provided important clues towards the identity of the host genes that conspire to promote post-integration latency of human immunodeficiency virus (HIV). Various genes controlling transcription, histone deacetylation and proteasome-mediated protein degradation have emerged as potential players. If the desired, but difficult, goal of complete virus eradication in HIV-infected patients is ever to be realized, the latent reservoir of HIV proviruses must be cleared. Understanding the molecular basis for viral latency is the key first step.

引用

收藏

页码：137 / 139

页数：3

相关论文

共 21 条

[1] Early establishment of a pool of latently infected, resting CD4+ T cells during primary HIV-1 infection [J].

Chun, TW ;

Engel, D ;

Berrey, MM ;

Shea, T ;

Corey, L ;

Fauci, AS .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (15) :8869-8873

[2] A point mutation in the HIV-1 Tat responsive element is associated with postintegration latency [J].

Emiliani, S ;

VanLint, C ;

Fischle, W ;

Paras, P ;

Ott, M ;

Brady, J ;

Verdin, E .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (13) :6377-6381

[3] Mutations in the tat gene are responsible for human immunodeficiency virus type 1 postintegration latency in the U1 cell line [J].

Emiliani, S ;

Fischle, W ;

Ott, M ;

Van Lint, C ;

Amella, CA ;

Verdin, E .

JOURNAL OF VIROLOGY, 1998, 72 (02) :1666-1670

[4] Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy [J].

Finzi, D ;

Blankson, J ;

Siliciano, JD ;

Margolick, JB ;

Chadwick, K ;

Pierson, T ;

Smith, K ;

Lisziewicz, J ;

Lori, F ;

Flexner, C ;

Quinn, TC ;

Chaisson, RE ;

Rosenberg, E ;

Walker, B ;

Gange, S ;

Gallant, J ;

Siliciano, RF .

NATURE MEDICINE, 1999, 5 (05) :512-517

[5] Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy [J].

Finzi, D ;

Hermankova, M ;

Pierson, T ;

Carruth, LM ;

Buck, C ;

Chaisson, RE ;

Quinn, TC ;

Chadwick, K ;

Margolick, J ;

Brookmeyer, R ;

Gallant, J ;

Markowitz, M ;

Ho, DD ;

Richman, DD ;

Siliciano, RF .

SCIENCE, 1997, 278 (5341) :1295-1300

[6] Counterregulation of chromatin deacetylation and histone deacetylase occupancy at the integrated promoter of human immunodeficiency virus type 1 (HIV-1) by the HIV-1 repressor YY1 and HIV-1 activator Tat [J].

He, GC ;

Margolis, DM .

MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (09) :2965-2973

[7] The site of HIV-1 integration in the human genome determines basal transcriptional activity and response to Tat transactivation [J].

Jordan, A ;

Defechereux, P ;

Verdin, E .

EMBO JOURNAL, 2001, 20 (07) :1726-1738

[8] ANTI-TERMINATION OF TRANSCRIPTION WITHIN THE LONG TERMINAL REPEAT OF HIV-1 BY TAT GENE-PRODUCT [J].

KAO, SY ;

CALMAN, AF ;

LUCIW, PA ;

PETERLIN, BM .

NATURE, 1987, 330 (6147) :489-493

[9] Host cell gene expression during human immunodeficiency virus type I latency and reactivation and effects of targeting genes that are differentially expressed in viral latency [J].

Krishnan, V ;

Zeichner, SL .

JOURNAL OF VIROLOGY, 2004, 78 (17) :9458-9473

[10] Expression of latent HAART-persistent HIV type 1 induced by novel cellular activating agents [J].

Kulkosky, J ;

Sullivan, J ;

Xu, Y ;

Souder, E ;

Hamer, DH ;

Pomerantz, RJ .

AIDS RESEARCH AND HUMAN RETROVIRUSES, 2004, 20 (05) :497-505