AI Article Synopsis
- Neonatal echovirus infections can lead to severe liver and brain complications, which may be fatal.
- The study identifies the human neonatal Fc receptor (hFcRn) and the lack of type I interferon (IFN) signaling as crucial factors that influence echovirus severity.
- Mice engineered to lack type I IFN signaling while expressing hFcRn demonstrate similar disease progression and liver damage as seen in human infections, providing a model for studying echovirus pathogenesis.
Article Abstract
Neonatal echovirus infections are characterized by severe hepatitis and neurological complications that can be fatal. Here, we show that expression of the human homologue of the neonatal Fc receptor (hFcRn), the primary receptor for echoviruses, and ablation of type I interferon (IFN) signaling are key host determinants involved in echovirus pathogenesis. We show that expression of hFcRn alone is insufficient to confer susceptibility to echovirus infections in mice. However, expression of hFcRn in mice deficient in type I interferon (IFN) signaling, hFcRn-IFNAR-/-, recapitulate the echovirus pathogenesis observed in humans. Luminex-based multianalyte profiling from E11 infected hFcRn-IFNAR-/- mice revealed a robust systemic immune response to infection, including the induction of type I IFNs. Furthermore, similar to the severe hepatitis observed in humans, E11 infection in hFcRn-IFNAR-/- mice caused profound liver damage. Our findings define the host factors involved in echovirus pathogenesis and establish in vivo models that recapitulate echovirus disease in humans.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7875378 | PMC |
| http://dx.doi.org/10.1371/journal.ppat.1009252 | DOI Listing |
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