Sun, Dec 21, 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: (49 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
References
1. Asseri AA. Respiratory Syncytial Virus: A Narrative Review of Updates and Recent Advances in Epidemiology, Pathogenesis, Diagnosis, Management and Prevention. J Clin Med. 2025;14(11):3880. [View at Publisher] [DOI] [PMID] [Google Scholar]
2. Chaumont A, Martin A, Flamaing J, Wiseman DJ, Vandermeulen C, Jongert E, et al. Host immune response to respiratory syncytial virus infection and its contribution to protection and susceptibility in adults: a systematic literature review. Expert Rev Clin Immunol. 2025;21(6):745-60. [View at Publisher] [DOI] [PMID] [Google Scholar]
3. Feldman C, Anderson R. RSV: an overview of infection in adults. Pneumonia. 2025;17(1):15. [View at Publisher] [DOI] [PMID] [Google Scholar]
4. Martín-Vicente M, González-Sanz R, Cuesta I, Monzón S, Resino S, Martínez I. Downregulation of A20 Expression Increases the Immune Response and Apoptosis and Reduces Virus Production in Cells Infected by the Human Respiratory Syncytial Virus. Vaccines (Basel). 2020;8(1):100. [View at Publisher] [DOI] [PMID] [Google Scholar]
5. Wu Y, He L, Li R, Li J, Zhao Q, Shao B. A20 as a Potential Therapeutic Target for COVID-19. Immun Inflamm Dis. 2025;13(1):e70127. [View at Publisher] [DOI] [PMID] [Google Scholar]
6. Sun Y, López CB. Preparation of Respiratory Syncytial Virus with High or Low Content of Defective Viral Particles and Their Purification from Viral Stocks. Bio Protoc. 2016;6(10):e1820. [View at Publisher] [DOI] [PMID] [Google Scholar]
7. Jiang X, Tian H, Fan Y, Chen J, Song Y, Wang S, et al. Expression of tumor necrosis factor alpha-induced protein 3 mRNA in peripheral blood mononuclear cells negatively correlates with disease severity in psoriasis vulgaris. Clin Vaccine Immunol. 2012;19(12):1938-42. [View at Publisher] [DOI] [PMID] [Google Scholar]
8. Catrysse L, Vereecke L, Beyaert R, van Loo G. A20 in inflammation and autoimmunity. Trends Immunol. 2014;35(1):22-31. [View at Publisher] [DOI] [PMID] [Google Scholar]
9. Maelfait J, Roose K, Bogaert P, Sze M, Saelens X, Pasparakis M, et al. A20 (Tnfaip3) Deficiency in Myeloid Cells Protects against Influenza A Virus Infection. PLoS Pathog. 2012;8(3):e1002570. [View at Publisher] [DOI] [PMID] [Google Scholar]
10. Martin-Vicente M, Mthiyane H, Jiménez-Sousa MA, Subramoney K, Hellferscee O, Wolter N, et al. TNFAIP3-interacting protein 1 polymorphisms and their association with symptomatic human respiratory syncytial virus infection and bronchiolitis in infants younger than one year from South Africa: A case-control study. Int J Infect Dis. 2023;136:107-10. [View at Publisher] [DOI] [PMID] [Google Scholar]
11. Priem D, Devos M, Druwé S, Martens A, Slowicka K, Ting AT, et al. A20 protects cells from TNF-induced apoptosis through linear ubiquitin-dependent and -independent mechanisms. Cell Death Dis. 2019;10(10):692. [View at Publisher] [DOI] [PMID] [Google Scholar]
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Contact us
Tel & Fax: (+98) 17-32450093
E-mail:
goums.ac.ir
yahoo.com