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1 May 2007

Volume 195, Number 9
The Journal of Infectious Diseases 2007;195:1303–1310
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2007/19509-0011$15.00
DOI: 10.1086/513438
MAJOR ARTICLE

Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis

Yoshihiko Hoshino,1

Satomi Hoshino,1

Jeffrey A. Gold,1

Bindu Raju,1

Savita Prabhakar,2

Richard Pine,2

William N. Rom,2

Koh Nakata,3 and

Michael Weiden2

1Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, New York; 2Public Health Research Institute (PHRI) and PHRI Tuberculosis Center, Newark, New Jersey; 3Niigata University Medical and Dental Hospital, Asahimachi‐Tohri, Niigata, Japan

Background.Pulmonary tuberculosis (TB) can present with polymorphonuclear neutrophil (PMN)–predominant alveolitis. TB accelerates acquired immunodeficiency syndrome by increasing human immunodeficiency virus type 1 (HIV‐1) replication and mutation in alveolar macrophages. A 16‐kDa CCAAAT/enhancer‐binding protein β (C/EBPβ) isoform is a strong transcriptional repressor of the HIV long terminal repeat (LTR) in resting alveolar macrophages, leading to latent viral infection; its expression is lost during TB, derepressing the HIV LTR.

Methods.Lung segments were sampled from HIV/Mycobacterium tuberculosis–coinfected patients by means of bronchoalveolar lavage. In vitro coculture experiments defined the mechanism of induction of HIV‐1 infection in macrophages by PMNs.

Results.Lung segments from patients with PMN‐predominant TB had a markedly elevated viral load. Direct contact between activated PMNs and macrophages stimulated HIV‐1 replication and LTR transcription and down‐regulated inhibitory C/EBPβ. Isolated PMN membranes substituted for PMN contact, derepressing the HIV‐1 LTR. The lipid raft fraction of PMN membranes expressed CD40 ligand (CD40L), CD28, and leukocyte function–associated antigen 1 (LFA‐1 [i.e., CD11a and CD18]), and PMN activation increased lipid raft expression of CD40L and CD28. Blocking antibodies to CD40L, CD28, and LFA‐1 inhibited PMN membrane–mediated HIV‐1 LTR derepression. Alternately, cross‐linking of macrophage receptors for CD40L, CD28, and LFA‐1 (CD40, CD80/86, and intercellular adhesion molecule 1) abolished inhibitory C/EBPβ expression.

Conclusion.PMN‐macrophage contact derepresses the HIV‐1 LTR and enhances HIV‐1 replication in alveolar macrophages during pulmonary TB. Derepression is mediated through costimulatory molecule signaling.

Received 1 September 2006; accepted 4 December 2006; electronically published 19 March 2007.

Reprints or correspondence: Dr. Michael Weiden, Div. of Pulmonary and Critical Medicine, Dept. of Medicine, New York University School of Medicine, 550 First Ave., New York, NY 10016 ().

Cited by

OA González, JL Ebersole, CB Huang. (2009) Oral infectious diseases: a potential risk factor for HIV virus recrudescence?. Oral Diseases 15:5, 313-327
Online publication date: 1-Aug-2009.
CrossRef

  • Potential conflicts of interest: none reported.

    Financial support: Japanese Foundation for AIDS Prevention; New York University Center for AIDS Research; National Institutes of Health (grants MO1 RR00096, HL57879, HL 59832, and DA022162).

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