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Received: 2004-06-01

Revision Accepted: 2005-01-17

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Journal of Zhejiang University SCIENCE B 2005 Vol.6 No.7 P.668-672


Extracellular HIV Tat and Tat cysteine rich peptide increase CCR5 expression in monocytes

Author(s):  ZHENG Lin, YANG Yi-da, LU Guo-cai, SALVATO Maria S.

Affiliation(s):  Department of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China; more

Corresponding email(s):   yidayang@hotmail.com

Key Words:  HIV Tat, Tat cysteine rich peptide, CCR5, Monocytes

ZHENG Lin, YANG Yi-da, LU Guo-cai, SALVATO Maria S.. Extracellular HIV Tat and Tat cysteine rich peptide increase CCR5 expression in monocytes[J]. Journal of Zhejiang University Science B, 2005, 6(7): 668-672.

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T1 - Extracellular HIV Tat and Tat cysteine rich peptide increase CCR5 expression in monocytes
A1 - ZHENG Lin
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A1 - LU Guo-cai
A1 - SALVATO Maria S.
J0 - Journal of Zhejiang University Science B
VL - 6
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DOI - 10.1631/jzus.2005.B0668

In our previous work we reported that HIV Tat and 6 cysteine rich peptides of Tat induce tumor necrosis factor-related apoptosis-induced ligand (TRAIL) in human monocytes (Yang et al., 2003). Here our results showed that HIV Tat and tat cysteine rich peptide increase CCR5 expression in human monocytes, and this activity is inhibited by rabbit anti-Tat. Boiled Tat does not increase CCR5 expression in monocytes. These results provide insight into a new mechanism by which HIV Tat plays a key role in the pathogenesis of HIV-1 infection.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


[1] Albini, A., Benelli, R., Giunciuglio, D., Cai, T., Mariani, G., Ferrini, S., Noonan, D.M., 1998. Identification of a novel domain of HIV Tat involved in monocyte chemotaxis. J. Biol. Chem., 273:15895-15900.

[2] Alkhatib, G., Combadiere, C., Broder, C.C., Feng, Y., Kennedy, P.E., Murphy, P.M., Berger, E.A., 1996. CC Ck5: A RANTES, MIP-1 alpha, MIP-1 beta receptor as a fusion cofactor for macrophage-tropic HIV-1. Science, 272:1955-1958.

[3] Barillari, G., Gendelman, R., Gallo, R.C., Ensoli, B., 1993. The Tat protein of human immunodeficiency virus type 1, a growth factor for AIDS Kaposi sarcoma and cytokine-activated vascular cells, induces adhesion of the same cell types by using integrin receptors recognizing the RGD amino acid sequence. Proc. Natl. Acad. Sci. USA, 90:7941-7945.

[4] Boykins, R.A., Mahieux, R., Shankavaram, U.T., Gho, Y.S., Lee, S.F., Hewlett, I.K., Wahl, L.M., Kleinman, H.K., Brady, J.N., Yamada, K.M., Dhawan, S., 1999. A short polypeptide domain of HIV-1-Tat protein mediates pathogenesis. J. Immunol, 163:15-20.

[5] Choe, H., Farzan, M., Sun, Y., Sullivan, N., Rollins, B., Ponath, P.D., Wu, L., Mackay, C.R., LaRosa, G., Newman, W., Gerard, N., Gerard, C., Sodroski, J., 1996. The beta-chemokine receptor CCR3 and CCR5 facilitate infection by primary HIV-1 isolates. Cell, 85:1135-1148.

[6] Huang, L., Bosch, I., Hoffmann, W., Sodroski, J., Pardee, A.B., 1998. Tat protein induces human immunodeficiency virus type 1 (HIV-1) coreceptors and promotes infection with both macrophage-tropic and T-lymphotropic HIV-1 strains. J. Virol., 72:8952-8960.

[7] Jeang, K.T., Xiao, H., Rich, E.A., 1999. Multifaceted activities of the HIV-1 transactivator of transcription, Tat. J. Biol. Chem., 27:28837-28840.

[8] Jons, K.A., 1993., Tat and HIV-1 promoter. Curr. Opin. Cell Biol., 5:461-468.

[9] Ott, M., Lee Lovett, J., Mueller, L., Verdin, E., 1998. Supperinduction of interleukine-8 in T cells by HIV Tat is mediated by NF-kB factors. J. Immunol, 160:2872-2880.

[10] Tikhonov, I., Ruckwardt, T.J., Hatfield, G.S., Pauza, C.D., 2003. Tat-neutralizing antibodies in vaccinated macaques. J. Virol., 77:3157-3166.

[11] Westendorp, M.O., Li-Weber, M., Frank, R.W., Krammer, P.H., 1994. Human immunodeficiency virus type 1 Tat up-regulates interleukin-2 secretion in activated T cells. J. Virol., 68:4177-4182.

[12] Westendorp, M.O., Frank, R., Ochsenbauer, C., Stricker, K., Dhein, J., Walczak, H., Debatin, K.M., Krammer, P.H., 1995. Sensitization of T cells to CD95-mediated apoptosis by HIV-Tat and gp120. Nature, 375:497-500.

[13] Yang, Y., Tikhonov, I., Ruckwardt, T., Djavani, M., Zapata, J.C., Pauza, C.D., Salvato, M.S., 2003. Monocytes treated with human immunodeficiency virus Tat kill uninfected CD4+ cells by a tumor necrosis factor related apoptosis induced ligand mediated mechanism. J. Virol., 77:6700-6708.

[14] Zauli, G., La Placa, M., Vignoli, M., Re, M.C., Gibellini, D., Furlini, G., Milani, D., Marchisio, M., Mazzoni, M., Capitani, S., 1995. An autocrine loop of HIV Tat protein responsible for the improved survival/proliferation capacity of permanently Tat-transfected cells and required for optimal human immunodeficiency virus type 1 long terminal repeat transactivating activity. J. Acquir. Immune. Defic. Syndr., 10:306-316.

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Chintan@No address<thejamboy@yahoo.com>

2011-02-21 15:08:23

good work

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