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Journal of Virology, December 2003, p. 12914-12920, Vol. 77, No. 23
0022-538X/03/$08.00+0 DOI: 10.1128/JVI.77.23.12914-12920.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Service de Neurovirologie,1 SPI-BIO, c/o Service de Neurovirologie, CEA, CRSSA, Université Paris Sud, EPHE, IPSC, Fontenay-aux-Roses,3 Unité de Biologie du Développement et de la Reproduction, Département de Physiologie Animale, Institut National de la Recherche Agronomique, Jouy-en-Josas, France2
Received 5 May 2003/ Accepted 20 August 2003
Tau interferon (IFN-
) is a noncytotoxic type I IFN responsible for maternal recognition of the fetus in ruminants. IFN-
inhibits human immunodeficiency virus (HIV) replication more strongly than human IFN-
, particularly in human monocyte-derived macrophages. In this study performed in human macrophages, IFN-
efficiently inhibited the early steps of the biological cycle of HIV, decreasing intracellular HIV RNA and inhibiting the initiation of the reverse transcription of viral RNA into proviral DNA. Two mechanisms induced by IFN-
treatment in macrophages may account for this inhibition: (i) the synthesis of the cellular antiviral factors such as 2',5'-oligoadenylate synthetase/RNase L and MxA protein and (ii) an increased production of MIP-1
, MIP-1ß, and RANTES, which are natural ligands of CCR5, the principal coreceptor of HIV on macrophages. Our results suggest that IFN-
induces the same antiviral pathways in macrophages as other type I IFNs but without associated toxicity.
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