Productive and persistent infection of human thymic epithelial cells in vitro with HIV-1

被引:28
作者
Braun, J
Valentin, H
Nugeyre, MT
Ohayon, H
Gounon, P
BarreSinoussi, F
机构
[1] INST PASTEUR,UNITE BIOL RETROVIRUS,DEPT VIROL,F-75724 PARIS 15,FRANCE
[2] INST PASTEUR,STN CENT MICROSCOPIE ELECT,F-75724 PARIS 15,FRANCE
关键词
D O I
10.1006/viro.1996.0617
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Infection with HIV-1 results in a disruption of the thymic microenvironment and the presence of HIV-1 in thymic epithelial cells has been demonstrated in vivo. In the present study, we examined the susceptibility of a highly enriched culture of thymic epithelial cells (TEC) to infection in vitro by HIV-1 laboratory strains and primary isolates. Replication in TEC is shown to depend on the virus and on the expression of CD4 molecules that are found to be expressed at a low density on the plasma membrane. Our results are consistent with infection of TEC controlled by the efficiency of the interactions between the envelope glycoprotein of the virus and the cell surface molecules. As a consequence, certain HIV-1 viruses induce a productive and persistent infection in TEC without damaging the cells. Altogether these results support the idea that TEC may act as a reservoir for HIV-1 in the thymus but are probably destroyed by an indirect mechanism involving infection of thymocytes. (C) 1996 Academic Press, Inc.
引用
收藏
页码:413 / 418
页数:6
相关论文
共 36 条
[1]   THE SCID-HU MOUSE AS A MODEL FOR HIV-1 INFECTION [J].
ALDROVANDI, GM ;
FEUER, G ;
GAO, LY ;
JAMIESON, B ;
KRISTEVA, M ;
CHEN, ISY ;
ZACK, JA .
NATURE, 1993, 363 (6431) :732-736
[2]   CC CKRS: A RANTES, MIP-1 alpha, MIP-1 beta receptor as a fusion cofactor for macrophage-tropic HIV-1 [J].
Alkhatib, G ;
Combadiere, C ;
Broder, CC ;
Feng, Y ;
Kennedy, PE ;
Murphy, PM ;
Berger, EA .
SCIENCE, 1996, 272 (5270) :1955-1958
[3]   Thymocyte and thymic microenvironment alterations during a systemic HIV infection in a severe combined immunodeficient mouse model [J].
Autran, B ;
Guiet, P ;
Raphael, M ;
Grandadam, M ;
Agut, H ;
Candotti, D ;
Grenot, P ;
Puech, F ;
Debre, P ;
Cesbron, JY .
AIDS, 1996, 10 (07) :717-727
[4]   HIV-1 INFECTIVITY OF HUMAN CARCINOMA CELL-LINES LACKING CD4 RECEPTORS [J].
BRICHACEK, B ;
DERDERIAN, C ;
CHERMANN, JC ;
HIRSCH, I .
CANCER LETTERS, 1992, 63 (01) :23-31
[5]   FREQUENT AND EARLY INUTERO HIV-1 INFECTION [J].
COURGNAUD, V ;
LAURE, F ;
BROSSARD, A ;
BIGNOZZI, C ;
GOUDEAU, A ;
BARIN, F ;
BRECHOT, C .
AIDS RESEARCH AND HUMAN RETROVIRUSES, 1991, 7 (03) :337-341
[6]  
DALLOUL AH, 1991, BLOOD, V77, P69
[7]  
DAVID FJE, 1992, CLIN EXP IMMUNOL, V88, P10
[8]   THE HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) GAG GENE-PRODUCT P18 IS RESPONSIBLE FOR ENHANCED FUSOGENICITY AND HOST RANGE TROPISM OF THE HIGHLY CYTOPATHIC HIV-1-NDK STRAIN [J].
DEMAREUIL, J ;
BRICHACEK, B ;
SALAUN, D ;
CHERMANN, JC ;
HIRSCH, I .
JOURNAL OF VIROLOGY, 1992, 66 (11) :6797-6801
[9]   Identification of a major co-receptor for primary isolates of HIV-1 [J].
Deng, HK ;
Liu, R ;
Ellmeier, W ;
Choe, S ;
Unutmaz, D ;
Burkhart, M ;
DiMarzio, P ;
Marmon, S ;
Sutton, RE ;
Hill, CM ;
Davis, CB ;
Peiper, SC ;
Schall, TJ ;
Littman, DR ;
Landau, NR .
NATURE, 1996, 381 (6584) :661-666
[10]   HIV-1 entry into CD4(+) cells is mediated by the chemokine receptor CC-CKR-5 [J].
Dragic, T ;
Litwin, V ;
Allaway, GP ;
Martin, SR ;
Huang, YX ;
Nagashima, KA ;
Cayanan, C ;
Maddon, PJ ;
Koup, RA ;
Moore, JP ;
Paxton, WA .
NATURE, 1996, 381 (6584) :667-673