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

Abstract

BACKGROUND 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. METHODS 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. RESULTS 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. CONCLUSION 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.

DOI: 10.1093/infdis/jit262
020040020132014201520162017
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@article{Chang2013HigherEO, title={Higher expression of several interferon-stimulated genes in HIV-1-infected females after adjusting for the level of viral replication.}, author={J Judy Chang and Matt Woods and Robert J Lindsay and Erin H Doyle and Morgane Griesbeck and Ellen S Chan and Gregory K Robbins and Ronald J Bosch and Marcus Altfeld}, journal={The Journal of infectious diseases}, year={2013}, volume={208 5}, pages={830-8} }