| First Author | Van Winkle JA | Year | 2018 |
| Journal | Cell Host Microbe | Volume | 24 |
| Issue | 5 | Pages | 665-676.e4 |
| PubMed ID | 30392829 | Mgi Jnum | J:267858 |
| Mgi Id | MGI:6269024 | Doi | 10.1016/j.chom.2018.10.003 |
| Citation | Van Winkle JA, et al. (2018) Persistence of Systemic Murine Norovirus Is Maintained by Inflammatory Recruitment of Susceptible Myeloid Cells. Cell Host Microbe 24(5):665-676.e4 |
| abstractText | Viral persistence can contribute to chronic disease and promote virus dissemination. Prior work demonstrated that timely clearance of systemic murine norovirus (MNV) infection depends on cell-intrinsic type I interferon responses and adaptive immunity. We now find that the capsid of the systemically replicating MNV strain CW3 promotes lytic cell death, release of interleukin-1alpha, and increased inflammatory cytokine release. Correspondingly, inflammatory monocytes and neutrophils are recruited to sites of infection in a CW3-capsid-dependent manner. Recruited monocytes and neutrophils are subsequently infected, representing a majority of infected cells in vivo. Systemic depletion of inflammatory monocytes or neutrophils from persistently infected Rag1(-/-) mice reduces viral titers in a tissue-specific manner. These data indicate that the CW3 capsid facilitates lytic cell death, inflammation, and recruitment of susceptible cells to promote persistence. Infection of continuously recruited inflammatory cells may be a mechanism of persistence broadly utilized by lytic viruses incapable of establishing latency. |
