Promotion of the resistance of human oral epithelial cells to herpes simplex virus type I infection via N6-methyladenosine modification

This study aimed to explore the mechanism behind N6-methyladenosine (m6A) modification of the total ribonucleic acid (RNA) involved in the resistance to herpes simplex virus type I (HSV-1) infection in oral epithelial cells. The variation in m6A modification level on messenger RNA following HSV-1 in...

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Bibliographic Details
Published in:BMC oral health 2023-02, Vol.23 (1), p.121-121, Article 121
Main Authors: Xu, Junping, Qi, Yuping, Ju, Qi
Format: Article
Language:English
Subjects:
alkb homolog 5
Alpha-Ketoglutarate-Dependent Dioxygenase FTO - genetics
Alpha-Ketoglutarate-Dependent Dioxygenase FTO - metabolism
Cell culture
Deoxyribonucleic acid
Development and progression
Dioxygenase
Disease resistance
DNA
Epigenetics
Epithelial cells
Epithelial Cells - metabolism
Fatty mass and obesity-associated gene
Fluorides
Gene expression
Genetic aspects
Health aspects
Herpes
Herpes simplex
Herpes Simplex - metabolism
Herpes simplex virus
Herpes simplex virus 1
Herpes viruses
Herpesvirus diseases
Humans
Infections
Interferon
Ketoglutaric acid
Kinases
m6A
Medical research
Medicine, Experimental
Methyltransferases
Mouth diseases
mRNA
N6-methyladenosine
Obesity
Oral herpes simplex
Physiology
Polymerase chain reaction
Proteins
Reagents
RNA - metabolism
RNA modification
RNA processing
Simplexvirus
siRNA
Type I interferon
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Summary:This study aimed to explore the mechanism behind N6-methyladenosine (m6A) modification of the total ribonucleic acid (RNA) involved in the resistance to herpes simplex virus type I (HSV-1) infection in oral epithelial cells. The variation in m6A modification level on messenger RNA following HSV-1 infection was determined using the RNA dot blot method. The expression levels of alpha-ketoglutarate-dependent dioxygenase lab homolog 5 (ALKBH5) protein and fatty mass and obesity-associated genes (FTO) were determined using real-time fluorescence quantification polymerase chain reaction and the western blot technique, respectively. Next, after suppressing the expression of ALKBH5 or FTO via small interfering RNA, human immortalised oral epithelial cells (HIOECs) were infected with HSV-1, followed by measurement of the viral load or expression level of type I interferon (I-IFN) and interferon-stimulated genes (ISGs). The m6A modification level was significantly increased following HSV-1 infection of the HIOECs (P 
ISSN:1472-6831
1472-6831
DOI:10.1186/s12903-023-02744-2