
HIV‐1 induces tumour necrosis factor and IL‐1 gene expression in primary human macrophages independent of productive infection
Author(s) -
HERBEIN G.,
KESHAV S.,
†OLLIN M.,
MONTANER L. J.,
GORDON S.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb07016.x
Subject(s) - tumor necrosis factor alpha , biology , macrophage , reverse transcriptase , microbiology and biotechnology , gene expression , beta (programming language) , virus , multiplicity of infection , immunology , cytokine , virology , in vitro , gene , polymerase chain reaction , biochemistry , computer science , programming language
SUMMARY Cylokines such as tumour necrosis factor‐alpha (TNF‐a) and IL‐Iβ may play a role in immunopalhogcncsis of AIDS, We studied early effects (05‐48 h) of monocytotropic (ADA) or tymp ho tropic (1MB) strains of HIV‐1 on TNF‐α and IL‐1β mRNA expression in primary human macrophages by a semi‐quantitative reverse transcriptase‐polymcrase chain reaction (RT‐PCR) assay. Three‐day‐old monocyte‐derived macrophages were exposed either to tissue culture supernatants containing virus (at multiplicity of infection (m.o.i.) of 005) or to control supernatants frceofvirionsandgpI20. ADA strain, but not IIIB. replicated in primary tissue culture‐differentiated macrophages (TCDM). Soluble CD4 (sC D4) was used to inhibit binding of both strains to macrophages. We found that TNF‐arand IL‐lβ gene expression was induced by both strains 0‐5‐3 hafter addition of virus, and that enhanced expression of both cytokines was inhibited by sCD4. We conclude that C D4‐dependcnl binding lo ihc cell surface is sufficient to enhance TNI′‐α and ll.‐lβ mRNA. whereas productive viral replication in primary human macrophages is not required. Therefore, similar pathways regulate gene expression of TNF‐a and IL‐Iβ by macrophages during initial infection by HIV‐1 in vitro .