AI Article Synopsis
- - Junín virus (JUNV) is a dangerous virus causing Argentine hemorrhagic fever (AHF), with its disease mechanisms not fully understood, but a high interferon-α (IFN-α) response correlates with worse outcomes.
- - Mice engineered to express the human transferrin receptor 1 (hTfR1) develop severe illness when infected with JUNV, marked by increased levels of serum IFN-α.
- - The study reveals that both the entry of JUNV through hTfR1 and the activation of the type I IFN response are crucial in causing severe disease in these mice, highlighting potential pathways for understanding and treating AHF.
Article Abstract
Junín virus (JUNV) is one of five New World mammarenaviruses (NWMs) that causes fatal hemorrhagic disease in humans and is the etiological agent of Argentine hemorrhagic fever (AHF). The pathogenesis underlying AHF is poorly understood; however, a prolonged, elevated interferon-α (IFN-α) response is associated with a negative disease outcome. A feature of all NWMs that cause viral hemorrhagic fever is the use of human transferrin receptor 1 (hTfR1) for cellular entry. Here, we show that mice expressing hTfR1 develop a lethal disease course marked by an increase in serum IFN-α concentration when challenged with JUNV. Further, we provide evidence that the type I IFN response is central to the development of severe JUNV disease in hTfR1 mice. Our findings identify hTfR1-mediated entry and the type I IFN response as key factors in the pathogenesis of JUNV infection in mice.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7297529 | PMC |
| http://dx.doi.org/10.7554/eLife.55352 | DOI Listing |
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