Zinc finger and interferon-stimulated genes play a vital role in TB-IRIS following HAART in AIDS

Author:

Ma Jinmin123,Zhao Fang4,Su Wei1,Li Qiongfang13,Li Jiandong13,Ji Jingkai13,Deng Yong4,Zhou Yang4,Wang Xinfa4,Yang Huanming15,Saksena Nitin K16,Kristiansen Karsten2,Wang Hui17,Liu Yingxia4

Affiliation:

1. BGI-Shenzhen, Shenzhen 518083, PR China

2. Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, Copenhagen 2100, Denmark

3. China National GeneBank, BGI-Shenzhen, Shenzhen 518120, PR China

4. Shenzhen Third People's Hospital, Shenzhen 518112, PR China

5. James D. Watson Institute of Genome Science, Hangzhou 310007, PR China

6. IGO, 19a Boundary Street, Rushcutters Bay, Sydney, NSW, Australia

7. Department of Engineering Science, University of Oxford, Oxford OX3 7DQ, UK

Abstract

Aim: Co-infection in HIV-1 patients with Mycobacterium tuberculosis poses considerable risk of developing the immune reconstitution inflammatory syndrome (IRIS), especially upon the initiation of antiretroviral therapy (ART). Methodology & results: For transcriptomic analysis, peripheral blood mononuclear cells’ whole gene expression was used from three patient groups: HIV+ (H), HIV-TB+ (HT), HIV-TB+ with IRIS (HTI). Pathway enrichment and functional analysis was performed before and after highly active ART. Genes in the interferon-stimulating and ZNF families maintained tight functional interaction and tilted the balance in favor of TB-IRIS. Discussion & conclusion: The functional impairment of interaction between ZNF genes and interferon-stimulated genes, along with higher expression of S100A8/S100A9 genes possibly forms the genomic basis of TB-IRIS in a subset of HIV patients while on highly active ART.

Publisher

Future Medicine Ltd

Subject

Pharmacology,Molecular Medicine,General Medicine

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