Productive HIV-1 infection is enriched in CD4-CD8- double negative (DN) T cells at pleural sites of dual infection with HIV and Mycobacterium tuberculosis

被引:0
作者
Qinglai Meng
David H. Canaday
David J. McDonald
Harriet Mayanja-Kizza
Joy Baseke
Zahra Toossi
机构
[1] Case Western Reserve University,Division of Infectious Diseases, Department of Medicine, BRB 10W
[2] Veterans Affairs Medical Center,Department of Molecular Biology and Microbiology
[3] Case Western Reserve University,undefined
[4] Makerere University,undefined
[5] Joint Clinical Research Center,undefined
来源
Archives of Virology | 2016年 / 161卷
关键词
T cell; Tuberculosis; HIV-1; PFMC; Double-negative T cell;
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摘要
A higher human immunodeficiency virus 1 (HIV-1) viral load at pleural sites infected with Mycobacterium tuberculosis (MTB) than in peripheral blood has been documented. However, the cellular source of productive HIV infection in HIV-1/MTB-coinfected pleural fluid mononuclear cells (PFMCs) remains unclear. In this study, we observed significant quantities of HIV-1 p24+ lymphocytes in PFMCs, but not in peripheral blood mononuclear cells (PBMCs). HIV-1 p24+ lymphocytes were mostly enriched in DN T cells. Intracellular CD4 expression was detectable in HIV-1 p24+ DN T cells. HIV-1 p24+ DN T cells showed lower surface expression of human leukocyte antigen (HLA)-ABC and tetherin than did HIV-1 p24+ CD4 T cells. Upon in vitro infection of PFMC CD4 T cells from TB mono-infected subjects, Nef- and/or Vpu-deleted HIV mutants showed lower generation of HIV-1 p24+ DN T cells than the wild-type virus. These data indicate that productively HIV-1-infected DN T cells, generated through down-modulation of surface CD4, likely by HIV-1 Nef and Vpu, are the predominant source of HIV-1 at pleural sites of HIV/MTB coinfection.
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页码:181 / 187
页数:6
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  • [1] Adachi A(1986)Production of acquired immunodeficiency syndrome-associated retrovirus in human and nonhuman cells transfected with an infectious molecular clone J Virol 59 284-291
  • [2] Gendelman HE(1994)Nef induces CD4 endocytosis: requirement for a critical dileucine motif in the membrane-proximal CD4 cytoplasmic domain Cell 76 853-864
  • [3] Koenig S(2001)Association between tuberculosis and HIV disease progression in a high tuberculosis prevalence area Int J Tuberc Lung Dis 5 225-232
  • [4] Folks T(1992)Crosslinking CD4 by human immunodeficiency virus gp120 primes T cells for activation-induced apoptosis J Exp Med 176 1099-1106
  • [5] Willey R(1993)Downregulation of cell-surface CD4 expression by simian immunodeficiency virus Nef prevents viral super infection J Exp Med 177 1561-1566
  • [6] Rabson A(1996)CD4 down-modulation during infection of human T cells with human immunodeficiency virus type 1 involves independent activities of vpu, env, and nef J Virol 70 6044-6053
  • [7] Martin MA(2002)Human immunodeficiency virus type 1 (HIV-1) quasispecies at the sites of J Virol 76 1697-1706
  • [8] Aiken C(2003) infection contribute to systemic HIV-1 heterogeneity Arch Intern Med 163 1009-1021
  • [9] Konner J(2000)The growing burden of tuberculosis: global trends and interactions with the HIV epidemic J Virol 74 8358-8367
  • [10] Landau NR(1999)Sensitivity of human immunodeficiency virus type 1 to the fusion inhibitor T-20 is modulated by coreceptor specificity defined by the V3 loop of gp120 JAMA 282 677-686