Knockout of the Tnfa Gene Decreases Influenza Virus-Induced Histological Reactions in Laboratory Mice

• Published in: International journal of molecular sciences 2024-01, Vol.25 (2), p.1156
• Main Authors: Savenkova, Darya A, Gudymo, Andrey S, Korablev, Alexey N, Taranov, Oleg S, Bazovkina, Darya V, Danilchenko, Nataliya V, Perfilyeva, Olga N, Ivleva, Elena K, Moiseeva, Anastasiya A, Bulanovich, Yulia A, Roshchina, Elena V, Serova, Irina A, Battulin, Nariman R, Kulikova, Elizabeth A, Yudkin, Dmitry V
• Format: Article
• Language: English
• Subjects: Animals; Brain; Chemokines; Cytokine storm; Cytokines - genetics; Dengue fever; Edema; Genomes; HIV; Human immunodeficiency virus; Infections; Influenza A virus; Lungs; Mice; Mice, Knockout; Orthomyxoviridae Infections - pathology; Proteins; Respiratory syncytial virus; Swine flu; Tumor Necrosis Factor-alpha - genetics; Tumor necrosis factor-TNF; Viral infections; Viruses
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms25021156

Tumor necrosis factor alpha (TNF-α) is a cytokine that is responsible for many processes associated with immune response and inflammation. It is involved in the development of an antiviral response to many virus infections. This factor was shown to be activated in influenza A virus infection, which enhances production of other cytokines. The overexpression of these cytokines can lead to a cytokine storm. To study the role of TNF-α in the development of pathologies associated with viral infection, we generated a knockout mouse strain. We demonstrated that these mice were characterized by a significant increase in the number of viral genomes compared to that in the parental strain, but the amount of live virus did not differ. A histopathology of the lungs in the genetically modified animals was significantly lower in terms of interalveolar septal infiltration. The generated model may be used to further study pathological processes in viral infections.