Aichi Virus Induces Antiviral Host Defense in Primary Murine Intestinal Epithelial Cells.
Yun-Te ChangMing-Hsiang KungThung-Hsien HsuWan-Ting HungYao-Shen ChenLi-Chen YenTsung-Hsien ChangPublished in: Viruses (2019)
The picornavirus Aichi virus (AiV) is a non-enveloped RNA virus that causes acute gastroenteritis symptoms, such as diarrhea, abdominal pain, nausea, vomiting, and fever. Antiviral host defense involves the fast response of type I interferon (IFN) and the secretion of inflammatory cytokines against pathogens. However, the intestinal inflammatory and antiviral response to AiV infection is poorly understood. This study evaluated the antiviral activity of intestinal epithelial cells (IECs), which form a single-cell layer separating the bowel wall from pathogens. Isolated primary mouse IECs were subjected to AiV infection and virion production, inducing the mRNA expression of type I/type III IFNs and inflammatory cytokines. The mechanism involved induced the expression of phospho-IFN regulatory factor 3 and mitochondrial antiviral-signaling protein of type I IFN signaling. These findings were also observed in AiV-infected human colon carcinoma cells. In summary, a viral productive and pathogenic infection of AiV in primary murine IECs is validated.
Keyphrases
- dendritic cells
- abdominal pain
- immune response
- type iii
- single cell
- oxidative stress
- endothelial cells
- poor prognosis
- transcription factor
- liver failure
- rna seq
- high glucose
- binding protein
- antimicrobial resistance
- high throughput
- hepatitis b virus
- physical activity
- intensive care unit
- long non coding rna
- multidrug resistant
- innate immune