Mon, Dec 22, 2025
1- Infectious Disease Research Center, Gonabad University of Medical Sciences, Gonabad, Iran.
2- Taleghani Children’s Hospital, Golestan University of Medical Sciences, Gorgan, Iran.
3- Department of Microbiology, Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran. ,alireza.tmn@gmail.com
2- Taleghani Children’s Hospital, Golestan University of Medical Sciences, Gorgan, Iran.
3- Department of Microbiology, Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran. ,
Abstract: (54 Views)
Introduction: Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections in infants and young children, with disease severity linked to excessive inflammation. A20 (TNFAIP3) is a negative regulator of NF‑κB signalling and may modulate RSV-induced lung inflammation. Here, we investigated the effect of RSV infection on pulmonary A20 gene expression in a murine model.
Methods: Female BALB/c mice (n=12; 6 per group) were intranasally infected with RSV (3 × 10⁶ PFU) and euthanized on day 5 post‑infection. Lung tissues were collected to analyse the A20 (TNFAIP3) mRNA expression 5 days following RSV infection by Real‑time RT‑PCR.
Results: Quantitative PCR analysis demonstrated a statistically significant upregulation of A20 expression in the lungs of RSV-infected mice compared to the uninfected control group 5 days following infection (p=0.0048).
Conclusions: RSV infection in mice induces A20 expression, suggesting a potential role for A20 in regulating pulmonary inflammation following the virus infection.
Methods: Female BALB/c mice (n=12; 6 per group) were intranasally infected with RSV (3 × 10⁶ PFU) and euthanized on day 5 post‑infection. Lung tissues were collected to analyse the A20 (TNFAIP3) mRNA expression 5 days following RSV infection by Real‑time RT‑PCR.
Results: Quantitative PCR analysis demonstrated a statistically significant upregulation of A20 expression in the lungs of RSV-infected mice compared to the uninfected control group 5 days following infection (p=0.0048).
Conclusions: RSV infection in mice induces A20 expression, suggesting a potential role for A20 in regulating pulmonary inflammation following the virus infection.
Keywords: Respiratory Syncytial Virus, Human, Tumor Necrosis Factor alpha-Induced Protein 3 (A20), NF-kappa B, Gene Expression Regulation, Mice
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