Amplification of HTLV-III/LAV infection by antigen-induced activation of T cells and direct suppression by virus of lymphocyte blastogenic responses

J. B. Margolick, D. J. Volkman, T. M. Folks, A. S. Fauci

Research output: Contribution to journalArticle

136 Citations (Scopus)

Abstract

Peripheral blood mononuclear cells (PBMNC) from healthy donors immune to the soluble antigens tetanus toxoid (TT) and/or keyhole limpet hemocyanin (KLH) were exposed to infectious human T lymphotropic virus, type III/lymphadenopathy-associated virus (HTLV-III/LAV) with and without prior activation by TT or KLH. After exposure to the virus, PBMNC that had been activated by antigen were 10 to 100 times more susceptible to viral replication, as estimated by measurement of production of reverse transcriptase and viral antigens, than PBMNC that had been preincubated without antigen. In addition, exposure of PBMNC to HTLV-III/LAV led to a loss of lymphocyte blastogenic responses after 2 to 3 wk in culture. HTLV-III/LAV-induced inhibition of lymphocyte blastogenic responses occurred in the absence of detectable production of RT but required the use of live rather than heat-inactivated virus. These results demonstrate that HTLV-III/LAV infection is amplified by antigen-induced activation of PBMNC, and that low levels of HTLV-III/LAV infection in vitro can suppress lymphocyte blastogenic responses. This study provides an in vitro model for the analysis of HTLV-III/LAV-induced immune defects.

Original languageEnglish (US)
Pages (from-to)1719-1723
Number of pages5
JournalJournal of Immunology
Volume138
Issue number6
StatePublished - 1987
Externally publishedYes

Fingerprint

CD27 Antigens
Virus Diseases
HIV
Lymphocytes
Viruses
Blood Cells
Antigens
Tetanus Toxoid
Viral Antigens
RNA-Directed DNA Polymerase

ASJC Scopus subject areas

  • Immunology

Cite this

Amplification of HTLV-III/LAV infection by antigen-induced activation of T cells and direct suppression by virus of lymphocyte blastogenic responses. / Margolick, J. B.; Volkman, D. J.; Folks, T. M.; Fauci, A. S.

In: Journal of Immunology, Vol. 138, No. 6, 1987, p. 1719-1723.

Research output: Contribution to journalArticle

@article{9528112368864ea7b1469bb47522f1f0,
title = "Amplification of HTLV-III/LAV infection by antigen-induced activation of T cells and direct suppression by virus of lymphocyte blastogenic responses",
abstract = "Peripheral blood mononuclear cells (PBMNC) from healthy donors immune to the soluble antigens tetanus toxoid (TT) and/or keyhole limpet hemocyanin (KLH) were exposed to infectious human T lymphotropic virus, type III/lymphadenopathy-associated virus (HTLV-III/LAV) with and without prior activation by TT or KLH. After exposure to the virus, PBMNC that had been activated by antigen were 10 to 100 times more susceptible to viral replication, as estimated by measurement of production of reverse transcriptase and viral antigens, than PBMNC that had been preincubated without antigen. In addition, exposure of PBMNC to HTLV-III/LAV led to a loss of lymphocyte blastogenic responses after 2 to 3 wk in culture. HTLV-III/LAV-induced inhibition of lymphocyte blastogenic responses occurred in the absence of detectable production of RT but required the use of live rather than heat-inactivated virus. These results demonstrate that HTLV-III/LAV infection is amplified by antigen-induced activation of PBMNC, and that low levels of HTLV-III/LAV infection in vitro can suppress lymphocyte blastogenic responses. This study provides an in vitro model for the analysis of HTLV-III/LAV-induced immune defects.",
author = "Margolick, {J. B.} and Volkman, {D. J.} and Folks, {T. M.} and Fauci, {A. S.}",
year = "1987",
language = "English (US)",
volume = "138",
pages = "1719--1723",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "6",

}

TY - JOUR

T1 - Amplification of HTLV-III/LAV infection by antigen-induced activation of T cells and direct suppression by virus of lymphocyte blastogenic responses

AU - Margolick, J. B.

AU - Volkman, D. J.

AU - Folks, T. M.

AU - Fauci, A. S.

PY - 1987

Y1 - 1987

N2 - Peripheral blood mononuclear cells (PBMNC) from healthy donors immune to the soluble antigens tetanus toxoid (TT) and/or keyhole limpet hemocyanin (KLH) were exposed to infectious human T lymphotropic virus, type III/lymphadenopathy-associated virus (HTLV-III/LAV) with and without prior activation by TT or KLH. After exposure to the virus, PBMNC that had been activated by antigen were 10 to 100 times more susceptible to viral replication, as estimated by measurement of production of reverse transcriptase and viral antigens, than PBMNC that had been preincubated without antigen. In addition, exposure of PBMNC to HTLV-III/LAV led to a loss of lymphocyte blastogenic responses after 2 to 3 wk in culture. HTLV-III/LAV-induced inhibition of lymphocyte blastogenic responses occurred in the absence of detectable production of RT but required the use of live rather than heat-inactivated virus. These results demonstrate that HTLV-III/LAV infection is amplified by antigen-induced activation of PBMNC, and that low levels of HTLV-III/LAV infection in vitro can suppress lymphocyte blastogenic responses. This study provides an in vitro model for the analysis of HTLV-III/LAV-induced immune defects.

AB - Peripheral blood mononuclear cells (PBMNC) from healthy donors immune to the soluble antigens tetanus toxoid (TT) and/or keyhole limpet hemocyanin (KLH) were exposed to infectious human T lymphotropic virus, type III/lymphadenopathy-associated virus (HTLV-III/LAV) with and without prior activation by TT or KLH. After exposure to the virus, PBMNC that had been activated by antigen were 10 to 100 times more susceptible to viral replication, as estimated by measurement of production of reverse transcriptase and viral antigens, than PBMNC that had been preincubated without antigen. In addition, exposure of PBMNC to HTLV-III/LAV led to a loss of lymphocyte blastogenic responses after 2 to 3 wk in culture. HTLV-III/LAV-induced inhibition of lymphocyte blastogenic responses occurred in the absence of detectable production of RT but required the use of live rather than heat-inactivated virus. These results demonstrate that HTLV-III/LAV infection is amplified by antigen-induced activation of PBMNC, and that low levels of HTLV-III/LAV infection in vitro can suppress lymphocyte blastogenic responses. This study provides an in vitro model for the analysis of HTLV-III/LAV-induced immune defects.

UR - http://www.scopus.com/inward/record.url?scp=0023098724&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023098724&partnerID=8YFLogxK

M3 - Article

C2 - 3493285

AN - SCOPUS:0023098724

VL - 138

SP - 1719

EP - 1723

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 6

ER -