HIV-1 preferentially infects M. tuberculosis-specific CD4+ T cells due to their increased production of IL-2

Alexandra Schuetz

Betts

Biancotto

Blatt

Brenchley

Brenna Hill

Bronke

Caruso

Casazza

Cheynier

Chou

Christof Geldmacher

Cocchi

Constantinos Petrovas

Cooper

David R. Ambrozak

Douek

Edwin J. Heeregrave

Elmar Saathoff

Erica Sanga

Finberg

Flynn

Gallegos

Gamadia

Geldmacher

Georgios Pollakis

Goletti

Griffin

Grossman

Hansen

Herbinger

Joseph P. Casazza

Kalsdorf

Kaufmann

Kinter

Klaus Reither

Komanduri

Leonard Maboko

Mario Roederer

Mark Louder

Mascola

Mattapallil

Mexas

Michael Hoelscher

Mogues

Murray

Njabulo Ngwenyama

Okoye

Paxton

Perfetto

Ramilo

Rana

Raszka

Richard A. Koup

Riedner

Slyker

Sonnenberg

Streitz

Tilton

Waldrop

William A. Paxton

William Ampofo

Zack

English

PubMed

HIV-1 infection results in the progressive loss of CD4 T cells. In this study, we address how different pathogen-specific CD4 T cells are affected by HIV infection and the cellular parameters involved. We found striking differences in the depletion rates between CD4 T cells to two common opportunistic pathogens, cytomegalovirus (CMV) and Mycobacterium tuberculosis (MTB). CMV-specific CD4 T cells persisted after HIV infection, whereas MTB-specific CD4 T cells were depleted rapidly. CMV-specific CD4 T cells expressed a mature phenotype and produced very little IL-2, but large amounts of MIP-1β. In contrast, MTB-specific CD4 T cells were less mature, and most produced IL-2 but not MIP-1β. Staphylococcal enterotoxin B-stimulated IL-2-producing cells were more susceptible to HIV infection in vitro than MIP-1β-producing cells. Moreover, IL-2 production was associated with expression of CD25, and neutralization of IL-2 completely abrogated productive HIV infection in vitro. HIV DNA was found to be most abundant in IL-2-producing cells, and least abundant in MIP-1β-producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis. These data support the hypothesis that differences in function affect the susceptibility of pathogen-specific CD4 T cells to HIV infection and depletion in vivo, providing a potential mechanism to explain the rapid loss of MTB-specific CD4 T cells after HIV infectio

Geldmacher, Christof

Ngwenyama, Njabulo

Schuetz, Alexandra

Petrovas, Constantinos

Reither, Klaus

Heeregrave, Edwin J.

Casazza, Joseph P.

Ambrozak, David R.

Louder, Mark

Ampofo, William

Pollakis, Georgios

Hill, Brenna

Sanga, Erica

Saathoff, Elmar

Maboko, Leonard

Roederer, Mario

Paxton, William A.

Hoelscher, Michael

Koup, Richard A.

NARCIS 

Preferential infection and depletion of Mycobacterium tuberculosis-specific CD4 T cells after HIV-1 infection

HIV-1 infection results in the progressive loss of CD4 T cells. In this study, we address how different pathogen-specific CD4 T cells are affected by HIV infection and the cellular parameters involved. We found striking differences in the depletion rates between CD4 T cells to two common opportunistic pathogens, cytomegalovirus (CMV) and Mycobacterium tuberculosis (MTB). CMV-specific CD4 T cells persisted after HIV infection, whereas MTB-specific CD4 T cells were depleted rapidly. CMV-specific CD4 T cells expressed a mature phenotype and produced very little IL-2, but large amounts of MIP-1β. In contrast, MTB-specific CD4 T cells were less mature, and most produced IL-2 but not MIP-1β. Staphylococcal enterotoxin B–stimulated IL-2–producing cells were more susceptible to HIV infection in vitro than MIP-1β–producing cells. Moreover, IL-2 production was associated with expression of CD25, and neutralization of IL-2 completely abrogated productive HIV infection in vitro. HIV DNA was found to be most abundant in IL-2–producing cells, and least abundant in MIP-1β–producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis. These data support the hypothesis that differences in function affect the susceptibility of pathogen-specific CD4 T cells to HIV infection and depletion in vivo, providing a potential mechanism to explain the rapid loss of MTB-specific CD4 T cells after HIV infection.</jats:p

Crossref

The Journal of Experimental Medicine

Preferential infection and depletion of Mycobacterium tuberculosis–specific CD4 T cells after HIV-1 infection

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Preferential infection and depletion of Mycobacterium tuberculosis–specific CD4 T cells after HIV-1 infection

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