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PMID: 9094699 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

55- and 75-kilodalton tumor necrosis factor receptors mediate distinct actions in regard to human immunodeficiency virus type 1 replication in primary human macrophages.

Journal of virology ·Vol. 71 ·No. 5 ·1997-05-00 ·Pages 4150-6

Herbein G, Gordon S

Abstract

We report in this study that repeated tumor necrosis factor alpha (TNF-alpha) pretreatment, starting before and continued after infection by human immunodeficiency virus type 1 (HIV-1), inhibits replication of the monocytotropic Ada strain in primary tissue culture-differentiated macrophages (TCDM), as assessed by sixfold lower levels of reverse transcriptase (RT) activity than that in untreated cells and absence of syncytium formation in TCDM cultures. In order to determine the pathways involved in inhibition of HIV-1 replication in primary TCDM pretreated with TNF-alpha, we tested TNF-alpha mutants T55 and T75, which recognize either the 55-kDa (TNF-R1) or the 75-kDa (TNF-R2) TNF receptor, respectively. Pretreatment of TCDM with the T75 mutant decreased the RT activity compared with that in untreated infected control cells fivefold and almost totally inhibited syncytium formation. In contrast, when TCDM were pretreated with the T55 mutant alone, syncytia were observed and RT activity was decreased about one-half. These results suggest that the inhibition of HIV-1 replication in TCDM pretreated with TNF-alpha might be mediated mainly through the 75-kDa TNF receptor (TNF-R2) rather than through the 55-kDa receptor (TNF-R1). Inhibition of HIV-1 replication in TCDM was observed with both T75 mutant pretreatment and posttreatment, starting at 1 h or 3 days after infection, whereas posttreatment with the T55 mutant, but not pretreatment, stimulated HIV-1 growth in primary TCDM. Both pre- and posttreatment with TNF-alpha inhibited HIV-1 replication in primary TCDM. The stimulation of HIV-1 replication by TNF-alpha in a chronically infected promonocytic cell line, U1, which contains two copies of integrated provirus, was mediated through the 55-kDa TNF-R1 alone and not through the 75-kDa TNF-R2. These results demonstrate that the 55-kDa TNF-R1 is involved in postintegration stimulation of HIV-1 while the 75-kDa TNF-R2 is involved in the inhibition of an early step of the viral life cycle in primary human TCDM.

MeSH Terms
Cell Line HIV-1/physiology Humans Macrophages/virology Molecular Weight Receptors, Tumor Necrosis Factor/physiology Tumor Necrosis Factor-alpha/pharmacology Virus Replication
Chemicals
Receptors, Tumor Necrosis Factor Tumor Necrosis Factor-alpha
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Herbein G
Virology Institute of the Faculty of Medicine and INSERM Unit 74, Louis Pasteur University, Strasbourg, France.
Gordon S
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
DOI
10.1128/JVI.71.5.4150-4156.1997
Published
1997-05-00
Pages
4150-6
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC191574
Subset
IM
External Links
PubMed source DOI: 10.1128/JVI.71.5.4150-4156.1997 PMC Full Text View journal details
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