IFN-stimulated gene expression is independent of the IFNL4 genotype in chronic HIV-1 infection

Katia Monteleone; Giuseppe Corano Scheri; Maura Statzu; Carla Selvaggi; Francesca Falasca; Noemi Giustini; Ivano Mezzaroma; Ombretta Turriziani; Gabriella d'Ettorre; Guido Antonelli; Carolina Scagnolari

doi:10.1007/s00705-016-3016-3

IFN-stimulated gene expression is independent of the IFNL4 genotype in chronic HIV-1 infection

Arch Virol. 2016 Nov;161(11):3263-8. doi: 10.1007/s00705-016-3016-3. Epub 2016 Aug 24.

Affiliations

¹ Laboratory of Virology, Department of Molecular Medicine, Istituto Pasteur Italia-Cenci Bolognetti Fondazione, Sapienza University of Rome, Viale di Porta Tiburtina n° 28, 00185, Rome, Italy.
² Department of Public Health and Infectious Diseases, Sapienza University of Rome, Rome, Italy.
³ Department of Clinical Medicine, Sapienza University of Rome, Rome, Italy.
⁴ Laboratory of Virology, Department of Molecular Medicine, Istituto Pasteur Italia-Cenci Bolognetti Fondazione, Sapienza University of Rome, Viale di Porta Tiburtina n° 28, 00185, Rome, Italy. carolina.scagnolari@uniroma1.it.

PMID: 27558125
DOI: 10.1007/s00705-016-3016-3

Abstract

This study aimed to evaluate the association between the IFNL4 rs368234815 (ΔG/TT) dinucleotide polymorphism and the IFN response during chronic HIV-1 infection. We carried out genotyping analysis and measured the expression of IFN-stimulated genes (ISGs) (myxovirus resistance protein A [MxA], ISG15, ISG56, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like [APOBEC] 3F and APOBEC3G) on peripheral blood mononuclear cells collected from naïve and HAART-treated HIV-1-infected patients. There were no statistically significant differences in endogenous ISGs mRNA levels among HIV-1-positive patients bearing different IFNL4 genotypes, suggesting that ISG expression is independent of the IFNL4 genotype in HIV-1 infection.

Keywords: HIV-1; IFN; IFNL4; ISGs; SNP.

MeSH terms

Adult
Female
Gene Expression Profiling*
Genotype*
Genotyping Techniques
HIV Infections / immunology*
Humans
Immunologic Factors / biosynthesis*
Interleukins / genetics*
Leukocytes, Mononuclear / immunology
Male
Middle Aged
Polymorphism, Genetic*
RNA, Messenger / analysis

Substances

IFNL4 protein, human
Immunologic Factors
Interleukins
RNA, Messenger