Investigation of the Mouse Infection Model for Echovirus 18

• Published in: Viruses Vol. 17; no. 7; p. 1011
• Main Authors: Xiang, Lei, Zhai, Linlin, Ou, Guanyong, Zhao, Wei, Yang, Yang, Shen, Chenguang
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 18.07.2025; MDPI
• Subjects: Animals; Antibodies; Aseptic meningitis; Brain - pathology; Brain - virology; Care and treatment; Children; Clinical isolates; Control; Diagnosis; Disease; Disease Models, Animal; Echovirus; echovirus 18; Echovirus Infections - pathology; Echovirus Infections - virology; Encephalitis; Encephalitis, Viral; Enterovirus B, Human - pathogenicity; Enteroviruses; Epidemics; Fatalities; Female; Genetic aspects; Health aspects; Identification and classification; IFNAR1 knockout mice; Infections; Measurement; Meningitis; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; mouse infection model; Muscle, Skeletal - pathology; Muscle, Skeletal - virology; Paralysis; pathogenesis; Pathogenicity; Receptor, Interferon alpha-beta - deficiency; Receptor, Interferon alpha-beta - genetics; Skeletal muscle; Testing; Transgenic animals; Vaccines; Viral antibodies; Viral infections; Viral Load; Viremia; Viruses; China; pathogenesis; IFNAR1 knockout mice; mouse infection model; viral load; echovirus 18
• ISSN: 1999-4915; 1999-4915
• DOI: 10.3390/v17071011

Echovirus 18, a member of the B group of enteroviruses, is a significant etiological agent of aseptic meningitis and viral encephalitis in children. In this study, we investigated the pathogenicity of E18 by establishing a mouse infection model after comparing various mouse strains and injection methods. Two-day-old IFNAR1 knockout mice infected with clinical isolates of E18 exhibited symptoms such as lethargy, hind limb paralysis, and even mortality. Similarly, some two-day-old C57BL/6J mice displayed comparable symptoms; however, the incidence was lower than that observed in IFNAR1 knockout mice. No similar symptoms were noted in any Balb/c mice. Significant pathological changes were observed in skeletal muscle, brain tissue, and other organs of symptomatic mice; among these tissues, skeletal muscle demonstrated the highest viral load. The established infection model using two-day-old IFNAR1 knockout mice provides valuable insights into further investigations regarding its pathological injury mechanisms as well as the protective effects conferred by antibodies.