The in vitro induction of human immunodeficiency virus (HIV) replication in purified protein derivative-positive HIV-infected persons by recall antigen response to Mycobacterium tuberculosis is the result of a balance of the effects of endogenous interleukin-2 and proinflammatory and antiinflammatory cytokines

Delia Goletti, Drew Weissman, Robert W. Jackson, Frank Collins, Audrey Kinter, Anthony S. Fauci

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is a serious problem, particularly in developing countries. Recently, M. tuberculosis and purified protein derivative (PPD) were demonstrated to induce HIV replication in CD8 T cell-depleted peripheral blood mononuclear cells from HIV-positive, PPD-positive persons but not in cells from PPD-negative persons. The role of endogenous and exogenous cytokines in modulating M. tuberculosis-induced HIV replication was evaluated. M. tuberculosis-induced HIV replication decreased following simultaneous inhibition of endogenous interleukin (IL)-2, IL-1β, and tumor necrosis factor-α by the addition of soluble receptors and receptor antagonists or following exogenous IL-10 and transforming growth factor (TGF)-β. In contrast, neutralization of endogenous IL-10 and TGF-β augmented M. tuberculosis-induced HIV replication by increasing cellular activation. Thus, the balance between IL-2 and proinflammatory and antiinflammatory cytokines plays a major role in M. tuberculosis-induced replication of HIV.

Original languageEnglish
Pages (from-to)1332-1338
Number of pages7
JournalJournal of Infectious Diseases
Volume177
Issue number5
Publication statusPublished - 1998

Fingerprint

Virus Replication
Mycobacterium tuberculosis
Interleukin-2
Anti-Inflammatory Agents
HIV
Cytokines
Antigens
Proteins
Transforming Growth Factors
Interleukin-10
In Vitro Techniques
Coinfection
Interleukin-1
Developing Countries
Blood Cells
Tumor Necrosis Factor-alpha
T-Lymphocytes

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

Cite this

@article{91a0854d0c6d4b27a184e237e10132ce,
title = "The in vitro induction of human immunodeficiency virus (HIV) replication in purified protein derivative-positive HIV-infected persons by recall antigen response to Mycobacterium tuberculosis is the result of a balance of the effects of endogenous interleukin-2 and proinflammatory and antiinflammatory cytokines",
abstract = "Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is a serious problem, particularly in developing countries. Recently, M. tuberculosis and purified protein derivative (PPD) were demonstrated to induce HIV replication in CD8 T cell-depleted peripheral blood mononuclear cells from HIV-positive, PPD-positive persons but not in cells from PPD-negative persons. The role of endogenous and exogenous cytokines in modulating M. tuberculosis-induced HIV replication was evaluated. M. tuberculosis-induced HIV replication decreased following simultaneous inhibition of endogenous interleukin (IL)-2, IL-1β, and tumor necrosis factor-α by the addition of soluble receptors and receptor antagonists or following exogenous IL-10 and transforming growth factor (TGF)-β. In contrast, neutralization of endogenous IL-10 and TGF-β augmented M. tuberculosis-induced HIV replication by increasing cellular activation. Thus, the balance between IL-2 and proinflammatory and antiinflammatory cytokines plays a major role in M. tuberculosis-induced replication of HIV.",
author = "Delia Goletti and Drew Weissman and Jackson, {Robert W.} and Frank Collins and Audrey Kinter and Fauci, {Anthony S.}",
year = "1998",
language = "English",
volume = "177",
pages = "1332--1338",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "5",

}

TY - JOUR

T1 - The in vitro induction of human immunodeficiency virus (HIV) replication in purified protein derivative-positive HIV-infected persons by recall antigen response to Mycobacterium tuberculosis is the result of a balance of the effects of endogenous interleukin-2 and proinflammatory and antiinflammatory cytokines

AU - Goletti, Delia

AU - Weissman, Drew

AU - Jackson, Robert W.

AU - Collins, Frank

AU - Kinter, Audrey

AU - Fauci, Anthony S.

PY - 1998

Y1 - 1998

N2 - Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is a serious problem, particularly in developing countries. Recently, M. tuberculosis and purified protein derivative (PPD) were demonstrated to induce HIV replication in CD8 T cell-depleted peripheral blood mononuclear cells from HIV-positive, PPD-positive persons but not in cells from PPD-negative persons. The role of endogenous and exogenous cytokines in modulating M. tuberculosis-induced HIV replication was evaluated. M. tuberculosis-induced HIV replication decreased following simultaneous inhibition of endogenous interleukin (IL)-2, IL-1β, and tumor necrosis factor-α by the addition of soluble receptors and receptor antagonists or following exogenous IL-10 and transforming growth factor (TGF)-β. In contrast, neutralization of endogenous IL-10 and TGF-β augmented M. tuberculosis-induced HIV replication by increasing cellular activation. Thus, the balance between IL-2 and proinflammatory and antiinflammatory cytokines plays a major role in M. tuberculosis-induced replication of HIV.

AB - Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is a serious problem, particularly in developing countries. Recently, M. tuberculosis and purified protein derivative (PPD) were demonstrated to induce HIV replication in CD8 T cell-depleted peripheral blood mononuclear cells from HIV-positive, PPD-positive persons but not in cells from PPD-negative persons. The role of endogenous and exogenous cytokines in modulating M. tuberculosis-induced HIV replication was evaluated. M. tuberculosis-induced HIV replication decreased following simultaneous inhibition of endogenous interleukin (IL)-2, IL-1β, and tumor necrosis factor-α by the addition of soluble receptors and receptor antagonists or following exogenous IL-10 and transforming growth factor (TGF)-β. In contrast, neutralization of endogenous IL-10 and TGF-β augmented M. tuberculosis-induced HIV replication by increasing cellular activation. Thus, the balance between IL-2 and proinflammatory and antiinflammatory cytokines plays a major role in M. tuberculosis-induced replication of HIV.

UR - http://www.scopus.com/inward/record.url?scp=0031948393&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031948393&partnerID=8YFLogxK

M3 - Article

VL - 177

SP - 1332

EP - 1338

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 5

ER -