HIV-1 and SIV Infection Are Associated with Early Loss of Lung Interstitial CD4+T Cells and Dissemination of Pulmonary Tuberculosis

被引：33

作者：

Corleis, Bjorn ^{[1
]}

Bucsan, Allison N. ^{[2
,3
]}

Deruaz, Maud ^{[1
,4
,5
]}

Vrbanac, Vladimir D. ^{[1
,4
,5
]}

Lisanti-Park, Antonella C. ^{[1
]}

Gates, Samantha J. ^{[1
]}

Linder, Alice H. ^{[1
]}

Paer, Jeffrey M. ^{[1
]}

Olson, Gregory S. ^{[1
]}

Bowman, Brittany A. ^{[1
]}

Schiff, Abigail E. ^{[1
]}

Medoff, Benjamin D. ^{[4
,5
,6
]}

Tager, Andrew M. ^{[1
,4
,5
,6
]}

Luster, Andrew D. ^{[4
,5
]}

Khader, Shabaana A. ^{[7
]}

Kaushal, Deepak ^{[2
,8
]}

Kwon, Douglas S. ^{[1
,9
]}

机构：

[1] Harvard Med Sch, Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Boston, MA 02115 USA

[2] Tulane Natl Primate Res Ctr, Covington, LA USA

[3] Tulane Univ, Sch Med, Dept Microbiol & Immunol, 1430 Tulane Ave, New Orleans, LA 70112 USA

[4] Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Charlestown, MA USA

[5] Harvard Med Sch, Charlestown, MA USA

[6] Massachusetts Gen Hosp, Div Pulm & Crit Care Med, Boston, MA 02114 USA

[7] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA

[8] Southwest Natl Primate Res Ctr, San Antonio, TX USA

[9] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA

来源：

CELL REPORTS | 2019年 / 26卷 / 06期

关键词：

IMMUNODEFICIENCY-VIRUS TYPE-1; CD4(+) T-CELLS; LATENT TUBERCULOSIS; EX-VIVO; ANTIRETROVIRAL THERAPY; RHESUS MACAQUES; DEPLETION; MECHANISMS; IMMUNITY; RISK;

D O I：

10.1016/j.celrep.2019.01.021

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Lung interstitial CD4+ T cells are critical for protection against pulmonary infections, but the fate of this population during HIV-1 infection is not well described. We studied CD4+ T cells in the setting of HIV-1 infection in human lung tissue, humanized mice, and a Mycobacterium tuberculosis (Mtb)/simian immunodeficiency virus (SIV) nonhuman primate co-infection model. Infection with a CCR5-tropic strain of HIV-1 or SIV results in severe and rapid loss of lung interstitial CD4+ T cells but not blood or lung alveolar CD4+ T cells. This is accompanied by high HIV-1 production in these cells in vitro and in vivo. Importantly, during early SIV infection, loss of lung interstitial CD4+ T cells is associated with increased dissemination of pulmonary Mtb infection. We show that lung interstitial CD4+ T cells serve as an efficient target for HIV-1 and SIV infection that leads to their early depletion and an increased risk of disseminated tuberculosis.

引用

页码：1409 / +

页数：15

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