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Microbiology and Immunology Publications
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|Type: ||Journal article|
|Title: ||HIV-1 infection of human macrophages directly induces viperin which inhibits viral production|
|Author: ||Nasr, Najla|
Harman, Andrew N.
Helbig, Karla Jayne
Bye, Chris R.
Wright, Thomas K.
Beard, Michael Robert
Cunningham, Anthony L.
|Citation: ||Blood, 2012; 120(4):778-788|
|Publisher: ||American Society of Hematology|
|Issue Date: ||2012|
|School/Discipline: ||School of Molecular and Biomedical Science : Microbiology and Immunology|
|Najla Nasr, Susan Maddocks, Stuart G. Turville, Andrew N. Harman, Natalie Woolger, Karla J.Helbig, John Wilkinson, Chris R. Bye, Thomas K. Wright, Dharshini Rambukwelle, Heather Donaghy, Michael R. Beard and Anthony L. Cunningham|
|Abstract: ||Macrophages are key target cells for HIV-1. HIV-1BaL induced a subset of interferon-stimulated genes in monocyte-derived macrophages (MDMs), which differed from that in monocyte-derived dendritic cells and CD4 T cells, without inducing any interferons. Inhibition of type I interferon induction was mediated by HIV-1 inhibition of interferon-regulated factor (IRF3) nuclear translocation. In MDMs, viperin was the most up-regulated interferon-stimulated genes, and it significantly inhibited HIV-1 production. HIV-1 infection disrupted lipid rafts via viperin induction and redistributed viperin to CD81 compartments, the site of HIV-1 egress by budding in MDMs. Exogenous farnesol, which enhances membrane protein prenylation, reversed viperin-mediated inhibition of HIV-1 production. Mutagenesis analysis in transfected cell lines showed that the internal S-adenosyl methionine domains of viperin were essential for its antiviral activity. Thus viperin may contribute to persistent noncytopathic HIV-1 infection of macrophages and possibly to biologic differences with HIV-1–infected T cells.|
|Rights: ||© 2012 by The American Society of Hematology|
|Appears in Collections:||Microbiology and Immunology Publications|
|View citing articles in: ||Web of Science|
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