Literature DB >> 23757341

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

J Judy Chang1, Matt Woods, Robert J Lindsay, Erin H Doyle, Morgane Griesbeck, Ellen S Chan, Gregory K Robbins, Ronald J Bosch, Marcus Altfeld.   

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.

Entities:  

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

Mesh:

Substances:

Year:  2013        PMID: 23757341      PMCID: PMC3733517          DOI: 10.1093/infdis/jit262

Source DB:  PubMed          Journal:  J Infect Dis        ISSN: 0022-1899            Impact factor:   5.226


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