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J Infect Dis. 2013 Sep 1;208(5):830-8. doi: 10.1093/infdis/jit262. Epub 2013 Jun 10.

Higher expression of several interferon-stimulated genes in HIV-1-infected females after adjusting for the level of viral replication.

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Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard, Harvard Medical School, Cambridge, MA 02139, USA.



Clinical studies have shown faster disease progression and stronger immune activation in human immunodeficiency virus (HIV)-1-infected females when compared with males for the same level of HIV-1 replication. Here we determine whether the elevated levels of HIV-1-induced interferon-alpha (IFN-α) production observed in females are associated with higher interferon-stimulated gene (ISG) expression levels in T cells, hence suggesting type-I IFN as a mechanism for the higher HIV-1-associated immune activation observed.


T-cell and dendritic cell populations were isolated from treatment-naive chronically HIV-1-infected individuals enrolled in the Adult Clinical Trials Group 384 by fluorescence-activated cell sorting. The expression of 98 genes involved in Toll-like receptor and type I IFN signaling pathways were quantified using Nanostring technology.


Several ISGs were significantly correlated with HIV-1 viral load and/or CD4(+) T-cell count. Higher expression levels of a subset of these ISGs were observed in cells derived from females as compared to males after adjusting for viral load and were correlated to higher levels of T-cell activation.


These data show that higher IFN-α production is associated with higher ex vivo expression of several ISGs in females. This might contribute to higher levels of immune activation and the observed faster HIV-1 disease progression in females for a given level of viral replication.


HIV-1; T cells; Toll-like receptors; dendritic cells; immune activation; innate immunity; pathogenesis; sex differences; type I Interferon

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