| Virus Name | Human adenovirus 3 |
| Virus Short Name | HAdV-5 |
| Order | Unassigned |
| Virus Family | Adenoviridae |
| Virus Subfamily | N.A. |
| Genus | Mastadenovirus |
| Species | Human mastadenovirus C |
| Host | Human, mammals |
| Cell Tropism | Epithelial cells |
| Associated Disease | Very common human infection, estimated to be responsible for between 2% and 5% of all respiratory infections. usually mild respiratory, gastrointestinal and eye infections. |
| Mode of Transmission | Respiratory, fecal-oral |
| VIPR DB link | N.A. |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/93/adenoviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Adenoviridae |
| Paper Title | Role of MyD88 in adenovirus keratitis |
| Author's Name | Xiaohong Zhou, Mirja Ramke, Ashish V. Chintakuntlawar, Jeong Yoon Lee, Jaya Rajaiya, and James Chodosh |
| Journal Name | Immunology Cell Biology |
| Pubmed ID | 27528076 |
| Abstract | Pattern recognition receptors (PRRs) are critical to the early detection and innate immune responses to pathogens. In particular, the toll-like receptor (TLR) system and its associated adaptor proteins have essential roles in early host responses to infection. Epidemic keratoconjunctivitis, caused by the human adenovirus, is a severe ocular surface infection associated with corneal inflammation (stromal keratitis). We previously showed that adenovirus capsid was a key molecular pattern in adenovirus keratitis, with viral DNA having a lesser role. We have now investigated the role of the adaptor molecule MyD88 in a mouse model of adenovirus keratitis in which there is no viral replication. In MyD88-/-Â mice infected with human adenovirus type 37, clinical keratitis was markedly reduced, along with infiltration of CD45+cells, and expression of inflammatory cytokines. Reduction of inflammatory cytokines was also observed in infected primary human corneal fibroblasts pretreated with a MyD88 inhibitory peptide. Keratitis similar to wild type mice was observed in TLR2, TLR9 and IL-1R knockout mice, but was reduced in TLR2/9 double knockout mice, consistent with synergy of TLR2 and TLR9 in the response to adenovirus infection. MyD88 co-immunoprecipitated with Src kinase in mice corneas and in human corneal fibroblasts infected with adenovirus, and MyD88 inhibitory peptide reduced Src phosphorylation, linking MyD88 activation to inflammatory gene expression through a signaling cascade previously shown to be directed by Src. Our findings reveal a critical role for the PRRs TLR2 and 9, and their adaptor protein MyD88, in corneal inflammation upon adenovirus infection. |
| Used Model | TLR2/9 double knockout mice |
| DOI | 10.1038/icb.2016.73 |
