Abstract |
Miltefosine (Milt) was originally synthesized as an antineoplastic agent but this phospholipid drug is now clinically used as an antiprotozoal compound. We demonstrate here that Milt reduces replication of HIV-1 in cocultures of human dendritic cells (DCs) and CD4(+) T cells. This phenomenon is due to a rapid secretion of soluble factors by DCs. We present evidence that the Milt-mediated repression in virus production is associated with induction of type-I interferon (IFN) in DCs. The Milt-dependent diminution in HIV-1 production was not totally abrogated by B18R, a vaccinia virus-encoded neutralizing type-I IFN receptor, which suggests the involvement of another yet to be identified soluble factor. Altogether, these results suggest that a therapy with Milt when used to control protozoan infections in individuals also carrying HIV-1 might also help to limit viral load. Additional studies are warranted to estimate the exact therapeutic potential of Milt as an anti-HIV-1 agent.
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Authors | Ravendra Garg, Michel J Tremblay |
Journal | Virology
(Virology)
Vol. 432
Issue 2
Pg. 271-6
(Oct 25 2012)
ISSN: 1096-0341 [Electronic] United States |
PMID | 22704066
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2012 Elsevier Inc. All rights reserved. |
Chemical References |
- Interferon Type I
- Phosphorylcholine
- miltefosine
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Topics |
- CD4-Positive T-Lymphocytes
(immunology, virology)
- Cell Line
- Coculture Techniques
- Dendritic Cells
(immunology)
- HIV-1
(drug effects, physiology)
- Humans
- Interferon Type I
(metabolism)
- Phosphorylcholine
(analogs & derivatives, pharmacology)
- Virus Replication
(drug effects)
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